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Cellular extensions

(Redirected fromCytoplasmic process)

Cellular extensionsalso known ascytoplasmic protrusionsandcytoplasmic processesare those structures that project from differentcells,in the body, or in other organisms. Many of the extensions arecytoplasmicprotrusions such as theaxonanddendriteof aneuron,known also as cytoplasmic processes.

Cellular extensions
This schematic illustrates the four different types ofglial cells,all of which possess cytoplasmic processes:ependymal cells(light pink),astrocytes(green),microglia(red), andoligodendrocytes(light blue).Cell bodiesofneuronsare in yellow (Theiraxonsare surrounded bymyelin,produced by oligodendrocytes).

Differentglial cellsproject cytoplasmic processes. In thebrain,the processes ofastrocytesform terminalendfeet,foot processesthat help to form protective barriers in the brain. In thekidneysspecialised cells calledpodocytesextend processes that terminate inpodocyte foot processesthat covercapillariesin thenephron.End-processes may also be known asvascular footplates,and in general may exhibit a pyramidal or finger-like morphology.[1][2]Mural cellssuch aspericytesextend processes to wrap aroundcapillaries.[2]

Foot-like processes are also present inMüller glia(modified astrocytes of theretina),[3]pancreatic stellate cells,[4]dendritic cells,[5]oligodendrocytes,[6]and others.Microglia,which are notably smaller thanmacroglia,can also extend their end-processes to contact areas of capillaries that are devoid ofastrocyte endfeet,and thereby contribute to the formation of theglia limitans.[7]

Other cellular extensions that protrude from thecell membraneare known asmembrane protrusionsor cell protrusions, also cell appendages, such asflagella,andmicrovilli.[8][9]Microtentaclesare cell protrusions attached to free-floating cells, associated with the spread of somecancer cells.[10]

Inprokaryotessuch protrusions are known as surface orcell-surface appendagesand includeflagella,pili,fimbriae,andnanowires.[11][8]Some archaea possess very complex appendages known ashami.[12]

Types

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Neuronal processes

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The cytoplasmic processes of a neuron are theaxonsanddendritesdifferentiated from the precursor neuronal processes known asneurites. [13]Adendritic spineis a membrane protrusion from a dendrite.

Glial processes

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The processes of glial cells include contractile processes, and processes inastrocytesthat terminate in foot processes known asendfeet.

Epithelial cell processes

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An illustration ofpodocytes,which surround theglomerular capillarieswith their cell bodies, primary processes and interdigitatingfoot processes.

Thepodocyteis a highly specialised epithelial cell inBowman's capsulein the kidney. Primary processes of the podocytes form terminal foot processes. Thepodocyte foot processeswrap around theglomerular capillariesin the kidney to function in the filtration barrier.

Foot processes vs. lamellipodia and filopodia

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The difference between foot processes, andlamellipodia,which are broad sheet-like protrusions, andfilopodia,which are long slender pointed extensions, is that lamellipodia and filopodia are especially significant forcell movement and migration,and they are "macro" membrane protrusions. In contrast, foot processes interact withbasement membranes,and are present at the "micro" scale.[1]

Filopodia and lamellipodia in two fluorescently-labeledgrowth cones.

However, cellular extensions, in general, can be found on a larger "macro" scale, occupying relatively large areas of thecell membrane.[1]For example, microglia can use their primary processes to constantly monitor and evaluate alterations in thebrainenvironment, and they can further deploy thinfilopodiafrom these primary processes to expand their surveillance area.[14]

Architectural similarities

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The arborization and branching of end-processes are one of the features responsible for the structural and functional similarities among various cell types.[note 1]Podocytesandpericytesshare many physiological properties due to their large surface areas and intricate network of primary and secondary processes that wrap around their associated capillaries.[15][16]

In addition, foot processes of podocytes anddendritic extensionsofneuronsexhibit comparable morphological features, and molecular machinery as they both share similar proteins found at bothsynapsesand foot processes, such assynaptopodinanddendrin.[17]This analogy between them is further supported by their shared vulnerability to pathological conditions such asAlzheimer's diseaseandminimal change nephropathy,both of which are characterized by reduction and damage of dendritic spines and foot processes respectively.[18]

Membrane protrusions

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Membrane protrusions or cell appendages, extend from thecell membrane,and includemicrovilli,cilia,andflagella.[9]Microvilli increase the surface area of atissue,such as from their abundance on tissue protrusions such asintestinal villi.

There is increasing evidence that membrane protrusions may act as platforms for the budding ofextracellular vesicles.[19]

Structure

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The cytoskeleton

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One key distinction between cellular processes and lamellipodia lies in the composition of theircytoskeletalelements. While cellular processes can be supported by any of the three major components of the cytoskeleton—microfilaments(actin filaments),intermediate filaments(IFs), ormicrotubules—, lamellipodia are primarily driven by thepolymerizationof actin microfilaments, not microtubules.[3][20]

Microtubules are generally unable to generate the force required by lamellipodia for large-scalecell movement,as this requires a significant number of microtubules to reach the cell'sleading edgein order to produce sufficient force to promote the development of significant protrusions and motility. As a result, lamellipodia are predominantly actin-based rather than microtubule-based.[20]

On the other hand, cellular processes can be:

  1. Radial microtubules:They are located in the proximal regions of the ramified processes of oligodendrocytes, that extend outward from the cell body.
  2. Lamellar microtubules:They are the microtubules that eventually wrap around the axon, forming themyelin sheath.
  • Actin-based:These include terminal foot processes of podocytes anddendritic spines(small protrusions arising from dendrites).[3]
  • IF-based:The predominant cytoskeletal element within astrocyte processes at birth is microtubules. However, as these cells mature, a significant shift occurs, with microtubules being almost completely replaced by intermediate filaments (IFs), composed predominantly ofglial fibrillary acidic protein(GFAP),[22]found in the end-feet of Müller cells and astrocytes.[23]

Numerous imaging methods, such asimmunohistochemistryandfluorescence microscopy,have enabled the precise targeting of, and are currently used to identify, visualize and localize specific marker proteins in foot processes, such asGFAPandsynaptopodin.Such techniques can be used to stain and study cells or identify relevant pathological changes.[3][24]

3D Structured illumination microscopy (SIM)enables visualisation of the glomerular filtration barrier, using multipleximmunofluorescencestaining for markers for podocytes (synaptopodin,nephrin),endothelial cells(EHD3), and theglomerular basement membrane(agrin).
Confocal microscopycan reveal changes in the processes ofMüller cells,in theretina,shown here in therat.On the left,GFAPexpression is predominant in theinner retinal layers.localized to the innermostlayers of the retina;on the right GFAP-positive fibers show a thickening in Müller cell processes indicatinggliosis.

The mitochondria

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In cells with unique architecture, energy requirements can vary significantly among different cellular compartments. As a result,mitochondria,within such cells, demonstrate a non-uniform distribution, and can be strategically localized in regions with the greatest energy needs.[25]

In order to support the substantial metabolic demands ofneurovascular coupling,astrocytic endfeet are loaded and packed with elongated and branched mitochondria.[26]This represents a marked departure from the typical pattern, wherein mitochondria generally tend to become smaller as their distance from the cell body increases, particularly within the fine branches and branchlets.[27]

However, while fine astrocytic perisynaptic processes can only house the smallest mitochondria, perivascular endfeet present a notable exception, and they can accommodate significantly more complex and ramified mitochondria.[27]In cases oftraumatic brain injuryand subsequentblood-brain barrierdisruption, there is even further augmentation in mitochondrial number and density within astrocytic endfeet in order to facilitatevascular remodelingas an adaptive response.[28]

On the contrary, foot processes of podocytes are devoid of mitochondria, and mitochondria are confined to thecytosolsurrounding thenucleus.The absence of mitochondria in foot processes can be attributed to the apparent size disparity, since mitochondria are generally larger than foot processes (The diameter of foot processes of normal podocytes can be under 250 nm).[25][29]

As a result, foot processes rely onglycolysisfor their energy supply, which may be beneficial as glycolysis offers the advantage of being unrestricted by a maximum capacity. Mitochondria, on the other hand, have a maximal limit, that renders them incapable of generating additional energy upon increased demand.[25]

Energy requirements of foot processes of podocytes

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Podocytes require a significant amount of energy to preserve the structural integrity of their foot processes, given the substantial mechanical stress they endure during the glomerular filtration process.[30]

Dynamic changes in glomerular capillary pressure exert both tensile and stretching forces on podocyte foot processes, and can lead to mechanical strain on theircytoskeleton.Concurrently, fluid flow shear stress is generated by the movement of glomerular ultrafiltrate, exerting a tangential force on the surface of these foot processes.[31]

In order to preserve their intricate foot process architecture, podocytes require a substantialATPexpenditure to maintain their structure and cytoskeletal organization, counteract the elevated glomerular capillary pressure and stabilize the capillary wall.[31]

It has also been suggested that podocytes may possess a reasonable degree of mobility along theglomerular basement membrane,a process that may also contribute to the high energy demand. Since filtered proteins may become entrapped and accumulate under podocyte cell body and major processes, a hypothesized strategy to facilitate the removal of these stagnant proteins involves a cyclical movement of podocytes, allowing trapped proteins to be dispersed from the subpodocyte space into the filtrate.[32]

Function

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End-processes are integral to the structure of diverse membranes and sheaths, and perivascular cells play a crucial role in the formation and maintenance of organ-blood barriers:[3][33]

The interface Associated end-processes
Theblood-brain barrierand theblood-spinal cord barrier Pericytes and astrocytes endfeet (Astrocytic endfeet envelop theabluminalsurface of brain capillaries, accounting for 70% to nearly 100% of their total surface area).[34]
Theinner blood retinal barrier(iBRB)[35] Pericytes and endfeet of glial cells like astrocytes and Müller cells.
Theglomerular filtration barrier Foot processes of podocytes.
Theglia limitans Astrocytic endfeet.
Themyelin sheath Oligodendrocytes.

Regulation of blood flow

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Cellular extensions of certain mural cells possess the capability to regulate the diameter of their associated blood vessels. Through the processes ofvasoconstrictionandvasodilation,these cells can actively control the rate of blood flow by means of:

Vasoactive modulators, released from astrocytic endfeet, act on smooth muscle cells in arterioles, and pericytes in capillaries to regulate thevascular tone.

Barrier and permeability regulation

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Podocytes, through their intricate network of foot processes, strictly control the passage ofplasma proteinsinto the urinary ultrafiltrate. Podocytes establish a selective barrier between their foot processes, allowing only molecules of appropriate size and charge to traverse. The negatively chargedglycocalyxcoating the foot processes facing the urinary space further enhances this barrier, creating anelectrostatic repulsionthat impedes the filtration ofalbumin.[37]

Glomerular podocytes possess a diverse array ofsurface-expressed proteinsthat contribute to the selective filtration of solutes across the glomerular barrier, thereby maintaining fluid homeostasis within the body.

Uptake and flux of ions, water and nutrients

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Astrocytic endfeet are rich in:

Cellular interaction

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Osteocytes

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Further information:Horizontal transfer of mitochondria

Thevascularizationofboneis a metabolically demanding process, requiring substantial energy to support the proliferation and migration ofendothelial cells.As a result,capillarieswhich arise from thebone marrow,and then pass through the cortical (outer) layer of bone, known as transcortical vessels (TCVs), require a robust supply ofmitochondriato facilitate vascular development.[41]

Osteocytes,the most common cell type withinmature cortical bone,actively participate in the growth and maintenance of TCVs through the transfer of mitochondria to endothelial cells.Scanning electron microscopyimages have revealed that osteocytes possess numerous dendritic processes with expanded, endfoot-like structures. These endfeet directly abut and communicate with TCVs, establishing a close physical association that enables the transfer of mitochondria, and thereby provide the endothelial cells with the energy necessary for vascularization.[41]

ThisSEMimage illustrates the communication between osteocytes (Ocy) and transcortical vessels (TCV) via their endfeet (yellow arrows) to facilitate mitochondrial transfer.

Pericytes

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Whilechemical signallingpathways have long been recognized as key mediators ofintercellular communication,recent studies have highlighted the significance of direct physical interactions in facilitating coordinated cellular responses. For example, pericyte secondary processes establish contact withendothelial cells,resulting in the formation ofpeg-socket invaginations,where pericyte processes extend inward, forming indentations within the endothelial cell membrane.[15]

During the process ofangiogenesis,newly formed microvessels typically consist of rapidly dividing endothelial cells and an immaturebasement membrane.Subsequent maturation of these microvessels involves the recruitment of pericytes. The presence of pericytes surrounding blood vessels is often associated with the inhibition of endothelial cell proliferation and the stabilization of newly formed microvessels.[42]

Indiabetic retinopathy(DR), accumulation of toxic substances such asadvanced glycation end-products(AGEs) leads to pericyte loss, weakening of capillary walls, andmicroaneurysms,all are hallmarks of DR. Abnormal changes in pericyte mechanical stiffness can impair their ability to maintain the arrest of capillary endothelial cell growth, which may be involved in angiogenesis,neovascularization,andproliferative DR.[43]

Cytotoxic T cells

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Traditionally,CD8+T-cells,responsible for combating intracellular pathogens, are required to undergo amulti-step migration processto reach infected organs. This process involves rolling along the endothelial surface, firm adhesion to the endothelium, and subsequent extravasation into the surrounding tissue. Nevertheless, in theliver,the fenestrated endothelium ofhepatic sinusoidsallows for direct contact between CD8+T-cells and thehepatocytes.[44]

In case ofviralorbacterialinfection of hepatocytes,plateletshave been observed to form clusters within the sinusoids of the liver and adhere to the surface of infectedKupffer cells.This aggregation is believed to serve as a mechanism for trapping pathogens and promoting their elimination by the immune system.[44]

CD8+T-cells, encountering platelet aggregates within liver sinusoids, are arrested and actively migrate along these sinusoids. They stretch out foot-like processes through the sinusoidal pores into thespace of Disse,and then scan hepatocytes for detection of infected cells.[note 2]Upon recognition ofantigens,these T cells initiatea cytotoxic responsecharacterized by producingcytokinesand killing infected cells without the need forextravasationinto theliver parenchyma.[44]

Microglia

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Microglia,while primarily known for theirimmunological functions,exhibit remarkable plasticity, enabling them to perform a diverse range of roles within thecentral nervous system.Traditionally, microglia have been characterized as existing in two distinct morphological states that correlate with changes in their functional properties:[45]

The ramified state The amoeboid state
Morphology Microglia are extensively branched with numerous primary and secondary processes. Microglia are rounded with compact cell body and retracted processes.
Physiological functions They scan the central nervous system, and establish contacts with neurons, astrocytes and blood vessels. Exhibiting a high degree of motility, they migrate to the lesion site and demonstrate a potentphagocyticcapacity for the clearance of debris and the elimination of pathogens.
Ramified microglia in a ratcortexbeforetraumatic brain injury.
Amoeboid microglia after traumatic brain injury.

Clinical significance

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Foot process effacement

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Foot process effacement(FPE) is a pathological condition, wherepodocyte foot processeswithdraw from their usual interdigitating position, retract into the primary processes of podocytes, and eventually fuse with the cell bodies, resulting in the formation of broad sheet-like extensions over theglomerular basement membrane(GBM).[46]

The podocyte cell bodies no longer maintain their typical position "floating" within the filtrate above the GBM. Instead, they become broadly adherent to it, resulting in the near-complete obliteration of the subpodocyte space, the region beneath the podocyte cell body and major processes.[46]

Effacement of foot processes (FP) of podocytes is evident in thisscanning electron microscopy(SEM) image, enhanced with false coloring for improved visualization.

FPE is a typical finding inproteinuricglomerular diseases, includingminimal change disease(MCD),membranous nephropathy,diabetic kidney disease,andIgA nephropathy.[47]FPE is hypothesized to be an adaptive mechanism in response to glomerular stress, rather than a mere consequence of cell injury and disease.[46]

For example, in inflammatory diseases such asanti-GBM glomerulonephritis,inflammatory mediators and the activation of thecomplement cascadecan damage the attachment of the actin cytoskeleton in foot processes to the GBM, thereby increasing the risk of podocyte detachment from the GBM.[46]

As a result, podocytes undergo cytoskeletal reorganization, resulting in the formation of a robust, basal cytoskeletal network that is tightly adhered to the GBM in order to minimize the risk of podocyte detachment. Even in cases of extensive FPE, recovery from effacement is possible if the disease resolves or with therapeutic intervention, and podocytes can restore their foot processes to their normal interdigitating state.[46]

Staphylococcus epidermidisinfections

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Staphylococcus epidermidis,a commonbacteriumfound as a normalcommensalonhuman skin,is a significant cause ofhospital-acquired infectionsthat are associated with the use ofimplanted medical deviceslikeheart valvesandcatheters.[48]

This bacterium can reach thebloodstreamas a contaminant from the skin, adhering to an implant using various mechanisms. In addition to producing aslimy substance,S. epidermidiscan anchor itself to the surface of the implant using foot-like processes.[49]These projections (appendages) extend from the bacterial cell wall and attach to the implant in linear arrangements, either singly or in multiples.[note 3]

Aquaporin-4

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Neuromyelitis optica spectrum disorder

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Neuromyelitis optica spectrum disorder(NMOSD) is anautoimmune inflammatory diseasecharacterized by the presence of serumantibodiesdirected against the water channel proteinaquaporin-4(AQP-4). These antibodies initiate a complement-dependent inflammatory cascade, culminating in tissue damage and destruction.[50][51]

Given that AQP4 is primarily expressed on perivascular astrocytic endfeet in thespinal cordand by Müller cells in theretina,NMOSD preferentially affects the spinal cord, and the anterior visual system.[50]

Patients with NMOSD typically exhibit worse visual acuity compared to those withmultiple sclerosis(MS), because NMOSD is primarily an inflammatory process targeting astrocytes, withdemyelinationas a secondary consequence. In contrast, MS primarily involves inflammatory demyelination.[51]

Since NMOSD targets Müller cells, which provide trophic support to the retina, and have a heightened expression of AQP4 in their endfeet facing blood vessels, it is evident that NMOSD can have a more severe impact on visual acuity.[51]

Alzheimer's disease

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AQP-4 exhibits a polarized distribution in astrocytes, with a 10-times higher concentration in astrocytic endfeet, which are in contact with blood vessels, compared to non-endfoot regions.[40]

In contrast to the lateral membranes of numerousepithelial cell types,astrocyte lateral membranes are devoid oftight junctions,that prevent diffusion of membrane molecules. In order to maintain their polarization and orientation towards blood vessels, AQP-4 channels must be securely anchored by specialized proteins.[40]

Recent studies have revealed a correlation between multiple neurological disorders, and the loss of AQP4 polarity (i.e. when AQP4 are widely distributed throughout the astrocyte, instead of its typical localization at the endfeet).[52]

AQP-4 facilitates the flow ofcerebrospinal fluidthrough thebrain parenchymafrom para-arterial to para-venous spaces, and thus AQP4 channels facilitate the clearance of waste products from the brain, thereby preventing their accumulation.[note 4]In Alzheimer's disease (AD), a disruption in the polarity of AQP4 can cause a buildup of waste products, such asamyloid betaandtau proteins,a defining characteristic of AD.[52]

This also explains why patients with NMSOD are at higher risk of developing AD, since damage of AQP4 in NMSOD may impair clearance of amyloid-beta.[53]

Epiretinal membrane

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Anepiretinal membrane(ERM) is an eye disease, where a greyish semi-translucent membrane progressively grows over themacula,leading to decreased visual acuity,metamorphopsia,and other complaints. ERM commonly occurs due toposterior vitreous detachment,which can cause a tear in theinternal limiting membrane(ILM), allowing microglial cells to migrate through the disrupted retinal architecture and interact with other cells at the vitreo-retinal interface, ultimately contributing to the formation of ERM.[54]

The standard surgical treatment for symptomatic ERMs ispars plana vitrectomywith membrane peel. However, despite the apparent complete removal of the ERM, there remains a risk ofrecurrence,which can be attributed to the presence of residual microscopic ERM remnants and the potential role of Müller cell footplates in the internal limiting membrane (ILM) in facilitating further cell proliferation and membrane formation. Minimising recurrence can therefore be achieved through peeling the underlying ILM together with the ERM.[55]

However, ILM peeling may result in the unintended damage of Müller cells, thereby increasing the risk of complications such as development of dissociated optic nerve fiber layer (DONFL), probably due to trauma to Müller cell footplate, and concomitant alterations in the nerve fiber layer and ganglion cell layer. As a result, intraoperativeoptical coherence tomography(iOCT)-guided ERM removal is an alternative approach that may minimize the risk of recurrence without the need for routine ILM peeling.[55]

Notes

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  1. ^This figureillustrates that end-processes of different cells can be considered analogous structures.
  2. ^This figureillustrates the formation of foot-like processes of CD8+T-cells upon encountering platelet aggregates.
  3. ^This figureillustrates the foot-like processes that S. epidermidis use to anchor itself to the surface of the implant.
  4. ^This figureillustrates the mechanism of AQP-4 dysfunction in Alzheimer's disease.

References

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  1. ^abcZhang, XA; Huang, C (September 2012)."Tetraspanins and cell membrane tubular structures".Cellular and Molecular Life Sciences.69(17):2843–52.doi:10.1007/s00018-012-0954-0.PMC10438980.PMID22450717.
  2. ^abGoddard, LM; Iruela-Arispe, ML (March 2013)."Cellular and molecular regulation of vascular permeability".Thrombosis and Haemostasis.109(3):407–15.doi:10.1160/TH12-09-0678.PMC3786592.PMID23389236.
  3. ^abcdeMescher, Anthony L. (2023).Junqueira's Basic Histology: Text and Atlas(17th ed.). McGraw-Hill Education.ISBN978-1264930395.
  4. ^Li, J; Chen, B; Fellows, GF; Goodyer, CG; Wang, R (2021)."Activation of Pancreatic Stellate Cells Is Beneficial for Exocrine but Not Endocrine Cell Differentiation in the Developing Human Pancreas".Frontiers in Cell and Developmental Biology.9:694276.doi:10.3389/fcell.2021.694276.PMC8418189.PMID34490247.Based on their star ( "stellate-like" ) shape with foot-like processes, PaSCs were found to surround cell clusters, ductal cells and newly formed islets, making complex cell-cell dendritic-like contacts.
  5. ^Lindquist, JA; Bernhardt, A; Reichardt, C; Sauter, E; Brandt, S; Rana, R; Lindenmeyer, MT; Philipsen, L; Isermann, B; Zhu, C; Mertens, PR (19 May 2023)."Cold Shock Domain Protein DbpA Orchestrates Tubular Cell Damage and Interstitial Fibrosis in Inflammatory Kidney Disease".Cells.12(10): 1426.doi:10.3390/cells12101426.PMC10217384.PMID37408260.In this context, dendritic cells within the renal interstitium are ideally positioned for immune surveillance, as their foot processes extend into the tubules, allowing them to take up antigens.
  6. ^Warren, AM; Grossmann, M; Christ-Crain, M; Russell, N (15 September 2023)."Syndrome of Inappropriate Antidiuresis: From Pathophysiology to Management".Endocrine Reviews.44(5):819–861.doi:10.1210/endrev/bnad010.PMC10502587.PMID36974717.The myelin sheath that protects axons is composed of foot processes of oligodendrocytes, supported by astrocytes that maintain homeostasis and form the blood-brain barrier.
  7. ^Barkaway, A; Attwell, D; Korte, N (July 2022)."Immune-vascular mural cell interactions: consequences for immune cell trafficking, cerebral blood flow, and the blood-brain barrier".Neurophotonics.9(3): 031914.doi:10.1117/1.NPh.9.3.031914.PMC9107322.PMID35581998.
  8. ^abOrbach, R; Su, X (2020)."Surfing on Membrane Waves: Microvilli, Curved Membranes, and Immune Signaling".Frontiers in Immunology.11:2187.doi:10.3389/fimmu.2020.02187.PMC7516127.PMID33013920.
  9. ^ab"Foundational Model of Anatomy - Cell appendage - Classes | NCBO BioPortal".bioportal.bioontology.org.Retrieved30 September2024.
  10. ^Killilea, AN; Csencsits, R; Le, EBNT; Patel, AM; Kenny, SJ; Xu, K; Downing, KH (15 August 2017)."Cytoskeletal organization in microtentacles".Experimental Cell Research.357(2):291–298.doi:10.1016/j.yexcr.2017.05.024.PMC5546326.PMID28551375.
  11. ^Bouhrour, N; Nibbering, PH; Bendali, F (8 May 2024)."Medical Device-Associated Biofilm Infections and Multidrug-Resistant Pathogens".Pathogens (Basel, Switzerland).13(5): 393.doi:10.3390/pathogens13050393.PMC11124157.PMID38787246.
  12. ^Moissl, Christine; Rachel, Reinhard; Briegel, Ariane; Engelhardt, Harald; Huber, Robert (2005-03-07)."The unique structure of archaeal 'hami', highly complex cell appendages with nano-grappling hooks: Unique structure of archaeal 'hami'".Molecular Microbiology.56(2):361–370.doi:10.1111/j.1365-2958.2005.04294.x.PMID15813730.S2CID31690026.
  13. ^Sainath, R; Gallo, G (January 2015)."Cytoskeletal and signaling mechanisms of neurite formation".Cell and Tissue Research.359(1):267–78.doi:10.1007/s00441-014-1955-0.PMC4286448.PMID25080065.
  14. ^Mayer, MG; Fischer, T (2024)."Microglia at the blood brain barrier in health and disease".Frontiers in Cellular Neuroscience.18:1360195.doi:10.3389/fncel.2024.1360195.PMC10976855.PMID38550920.
  15. ^abDessalles, CA; Babataheri, A; Barakat, AI (22 March 2021)."Pericyte mechanics and mechanobiology".Journal of Cell Science.134(6).doi:10.1242/jcs.240226.PMID33753399.
  16. ^Del Pinto, R; Mulè, G; Vadalà, M; Carollo, C; Cottone, S; Agabiti Rosei, C; De Ciuceis, C; Rizzoni, D; Ferri, C; Muiesan, ML (25 May 2022)."Arterial Hypertension and the Hidden Disease of the Eye: Diagnostic Tools and Therapeutic Strategies".Nutrients.14(11): 2200.doi:10.3390/nu14112200.PMC9182467.PMID35683999.
  17. ^Caza, TN; Al-Rabadi, LF; Beck LH, Jr (2021)."How Times Have Changed! A Cornucopia of Antigens for Membranous Nephropathy".Frontiers in Immunology.12:800242.doi:10.3389/fimmu.2021.800242.PMC8662735.PMID34899763.
  18. ^Badeński, A; Badeńska, M; Świętochowska, E; Didyk, A; Morawiec-Knysak, A; Szczepańska, M (14 October 2022)."Assessment of Brain-Derived Neurotrophic Factor (BDNF) Concentration in Children with Idiopathic Nephrotic Syndrome".International Journal of Molecular Sciences.23(20): 12312.doi:10.3390/ijms232012312.PMC9603999.PMID36293164.
  19. ^Rilla, K (September 2021)."Diverse plasma membrane protrusions act as platforms for extracellular vesicle shedding".Journal of Extracellular Vesicles.10(11): e12148.doi:10.1002/jev2.12148.PMC8448080.PMID34533887.
  20. ^abHohmann, T; Dehghani, F (18 April 2019)."The Cytoskeleton-A Complex Interacting Meshwork".Cells.8(4): 362.doi:10.3390/cells8040362.PMC6523135.PMID31003495.
  21. ^Sun, H; Perez-Gill, C; Schlöndorff, JS; Subramanian, B; Pollak, MR (February 2021)."Dysregulated Dynein-Mediated Trafficking of Nephrin Causes INF2-related Podocytopathy".Journal of the American Society of Nephrology.32(2):307–322.doi:10.1681/ASN.2020081109.PMC8054882.PMID33443052.
  22. ^abWeigel, M; Wang, L; Fu, MM (April 2021)."Microtubule organization and dynamics in oligodendrocytes, astrocytes, and microglia".Developmental Neurobiology.81(3):310–320.doi:10.1002/dneu.22753.PMID32324338.
  23. ^Ziółkowska, N; Lewczuk, B; Szyryńska, N; Rawicka, A; Vyniarska, A (26 March 2023)."Low-Intensity Blue Light Exposure Reduces Melanopsin Expression in Intrinsically Photosensitive Retinal Ganglion Cells and Damages Mitochondria in Retinal Ganglion Cells in Wistar Rats".Cells.12(7): 1014.doi:10.3390/cells12071014.PMC10093228.PMID37048087.
  24. ^Gyarmati, G; Shroff, UN; Riquier-Brison, A; Kriz, W; Kaissling, B; Neal, CR; Arkill, KP; Ahmadi, N; Gill, IS; Moon, JY; Desposito, D; Peti-Peterdi, J (1 March 2021)."A new view of macula densa cell microanatomy".American Journal of Physiology. Renal Physiology.320(3):F492 –F504.doi:10.1152/ajprenal.00546.2020.PMC7988809.PMID33491562.
  25. ^abcOzawa, S; Ueda, S; Imamura, H; Mori, K; Asanuma, K; Yanagita, M; Nakagawa, T (18 December 2015)."Glycolysis, but not Mitochondria, responsible for intracellular ATP distribution in cortical area of podocytes".Scientific Reports.5:18575.Bibcode:2015NatSR...518575O.doi:10.1038/srep18575.PMC4683464.PMID26677804.
  26. ^Novorolsky, RJ; Kasheke, GDS; Hakim, A; Foldvari, M; Dorighello, GG; Sekler, I; Vuligonda, V; Sanders, ME; Renden, RB; Wilson, JJ; Robertson, GS (2023)."Preserving and enhancing mitochondrial function after stroke to protect and repair the neurovascular unit: novel opportunities for nanoparticle-based drug delivery".Frontiers in Cellular Neuroscience.17:1226630.doi:10.3389/fncel.2023.1226630.PMC10360135.PMID37484823.
  27. ^abBergami, M; Motori, E (2020)."Reweaving the Fabric of Mitochondrial Contact Sites in Astrocytes".Frontiers in Cell and Developmental Biology.8:592651.doi:10.3389/fcell.2020.592651.PMC7649784.PMID33195262.
  28. ^Gӧbel, J; Engelhardt, E; Pelzer, P; Sakthivelu, V; Jahn, HM; Jevtic, M; Folz-Donahue, K; Kukat, C; Schauss, A; Frese, CK; Giavalisco, P; Ghanem, A; Conzelmann, KK; Motori, E; Bergami, M (7 April 2020)."Mitochondria-Endoplasmic Reticulum Contacts in Reactive Astrocytes Promote Vascular Remodeling".Cell Metabolism.31(4): 791–808.e8.doi:10.1016/j.cmet.2020.03.005.PMC7139200.PMID32220306.
  29. ^Siegerist, F; Drenic, V; Koppe, TM; Telli, N; Endlich, N (January 2023)."Super-Resolution Microscopy: A Technique to Revolutionize Research and Diagnosis of Glomerulopathies".Glomerular Diseases.3(1):19–28.doi:10.1159/000528713.PMC9936760.PMID36816428.
  30. ^Baek, J; Lee, YH; Jeong, HY; Lee, SY (September 2023)."Mitochondrial quality control and its emerging role in the pathogenesis of diabetic kidney disease".Kidney Research and Clinical Practice.42(5):546–560.doi:10.23876/j.krcp.22.233.PMC10565453.PMID37448292.
  31. ^abBlaine, J; Dylewski, J (16 July 2020)."Regulation of the Actin Cytoskeleton in Podocytes".Cells.9(7): 1700.doi:10.3390/cells9071700.PMC7408282.PMID32708597.
  32. ^Welsh, GI; Saleem, MA (25 October 2011)."The podocyte cytoskeleton--key to a functioning glomerulus in health and disease".Nature Reviews. Nephrology.8(1):14–21.doi:10.1038/nrneph.2011.151.PMID22025085.
  33. ^Caceres, PS; Benedicto, I; Lehmann, GL; Rodriguez-Boulan, EJ (1 March 2017)."Directional Fluid Transport across Organ-Blood Barriers: Physiology and Cell Biology".Cold Spring Harbor Perspectives in Biology.9(3): a027847.doi:10.1101/cshperspect.a027847.PMC5334253.PMID28003183.
  34. ^abDíaz-Castro, B; Robel, S; Mishra, A (10 July 2023)."Astrocyte Endfeet in Brain Function and Pathology: Open Questions".Annual Review of Neuroscience.46:101–121.doi:10.1146/annurev-neuro-091922-031205.hdl:20.500.11820/c7641ed1-a889-4f3d-941e-1100fd631989.PMID36854317.
  35. ^Peña, JS; Vazquez, M (30 May 2022)."Harnessing the Neuroprotective Behaviors of Müller Glia for Retinal Repair".Frontiers in Bioscience (Landmark Edition).27(6): 169.doi:10.31083/j.fbl2706169.PMC9639582.PMID35748245.
  36. ^Bergers, G; Song, S (October 2005)."The role of pericytes in blood-vessel formation and maintenance".Neuro-oncology.7(4):452–64.doi:10.1215/S1152851705000232.PMC1871727.PMID16212810.
  37. ^Reiser, J; Altintas, MM (2016)."Podocytes".F1000Research.5:114.doi:10.12688/f1000research.7255.1.PMC4755401.PMID26918173.
  38. ^Zhang, YM; Qi, YB; Gao, YN; Chen, WG; Zhou, T; Zang, Y; Li, J (2023)."Astrocyte metabolism and signaling pathways in the CNS".Frontiers in Neuroscience.17:1217451.doi:10.3389/fnins.2023.1217451.PMC10507181.PMID37732313.
  39. ^Roth, W; Zadeh, K; Vekariya, R; Ge, Y; Mohamadzadeh, M (15 March 2021)."Tryptophan Metabolism and Gut-Brain Homeostasis".International Journal of Molecular Sciences.22(6): 2973.doi:10.3390/ijms22062973.PMC8000752.PMID33804088.
  40. ^abcNagelhus, EA; Ottersen, OP (October 2013)."Physiological roles of aquaporin-4 in brain".Physiological Reviews.93(4):1543–62.doi:10.1152/physrev.00011.2013.PMC3858210.PMID24137016.
  41. ^abLiao, P; Chen, L; Zhou, H; Mei, J; Chen, Z; Wang, B; Feng, JQ; Li, G; Tong, S; Zhou, J; Zhu, S; Qian, Y; Zong, Y; Zou, W; Li, H; Zhang, W; Yao, M; Ma, Y; Ding, P; Pang, Y; Gao, C; Mei, J; Zhang, S; Zhang, C; Liu, D; Zheng, M; Gao, J (21 March 2024)."Osteocyte mitochondria regulate angiogenesis of transcortical vessels".Nature Communications.15(1): 2529.Bibcode:2024NatCo..15.2529L.doi:10.1038/s41467-024-46095-0.PMC10957947.PMID38514612.
  42. ^Geevarghese, A; Herman, IM (April 2014)."Pericyte-endothelial crosstalk: implications and opportunities for advanced cellular therapies".Translational Research.163(4):296–306.doi:10.1016/j.trsl.2014.01.011.PMC3976718.PMID24530608.
  43. ^Hammes, HP; Lin, J; Renner, O; Shani, M; Lundqvist, A; Betsholtz, C; Brownlee, M; Deutsch, U (October 2002)."Pericytes and the pathogenesis of diabetic retinopathy".Diabetes.51(10):3107–12.doi:10.2337/diabetes.51.10.3107.PMID12351455.
  44. ^abcGuidotti, LG; Inverso, D; Sironi, L; Di Lucia, P; Fioravanti, J; Ganzer, L; Fiocchi, A; Vacca, M; Aiolfi, R; Sammicheli, S; Mainetti, M; Cataudella, T; Raimondi, A; Gonzalez-Aseguinolaza, G; Protzer, U; Ruggeri, ZM; Chisari, FV; Isogawa, M; Sitia, G; Iannacone, M (23 April 2015)."Immunosurveillance of the liver by intravascular effector CD8(+) T cells".Cell.161(3):486–500.doi:10.1016/j.cell.2015.03.005.hdl:10281/89208.PMID25892224.
  45. ^Vidal-Itriago, A; Radford, RAW; Aramideh, JA; Maurel, C; Scherer, NM; Don, EK; Lee, A; Chung, RS; Graeber, MB; Morsch, M (2022)."Microglia morphophysiological diversity and its implications for the CNS".Frontiers in Immunology.13:997786.doi:10.3389/fimmu.2022.997786.PMC9627549.PMID36341385.
  46. ^abcdeKriz, W; Shirato, I; Nagata, M; LeHir, M; Lemley, KV (15 February 2013)."The podocyte's response to stress: the Enigma of foot process effacement".American Journal of Physiology. Renal Physiology.304(4): F333-47.doi:10.1152/ajprenal.00478.2012.PMID23235479.
  47. ^Deegens, JK; Dijkman, HB; Borm, GF; Steenbergen, EJ; van den Berg, JG; Weening, JJ; Wetzels, JF (December 2008)."Podocyte foot process effacement as a diagnostic tool in focal segmental glomerulosclerosis".Kidney International.74(12):1568–76.doi:10.1038/ki.2008.413.PMID18813290.
  48. ^Lee, E; Anjum, F (January 2024),"Staphylococcus epidermidis Infection.",StatPearls,Treasure Island, Florida (FL): StatPearls Publishing,PMID33085387
  49. ^Franson, TR; Sheth, NK; Rose, HD; Sohnle, PG (September 1984)."Scanning electron microscopy of bacteria adherent to intravascular catheters".Journal of Clinical Microbiology.20(3):500–5.doi:10.1128/jcm.20.3.500-505.1984.PMC271359.PMID6490834.
  50. ^abKleerekooper, I; Houston, S; Dubis, AM; Trip, SA; Petzold, A (2020)."Optical Coherence Tomography Angiography (OCTA) in Multiple Sclerosis and Neuromyelitis Optica Spectrum Disorder".Frontiers in Neurology.11:604049.doi:10.3389/fneur.2020.604049.PMC7758345.PMID33362705.
  51. ^abcGigengack, NK; Oertel, FC; Motamedi, S; Bereuter, C; Duchow, A; Rust, R; Bellmann-Strobl, J; Ruprecht, K; Schmitz-Hübsch, T; Paul, F; Brandt, AU; Zimmermann, HG (20 October 2022)."Structure-function correlates of vision loss in neuromyelitis optica spectrum disorders".Scientific Reports.12(1): 17545.Bibcode:2022NatSR..1217545G.doi:10.1038/s41598-022-19848-4.PMC9585067.PMID36266394.
  52. ^abMader, S; Brimberg, L (27 January 2019)."Aquaporin-4 Water Channel in the Brain and Its Implication for Health and Disease".Cells.8(2): 90.doi:10.3390/cells8020090.PMC6406241.PMID30691235.
  53. ^Cho, EB; Jung, SY; Jung, JH; Yeo, Y; Kim, HJ; Han, K; Shin, DW; Min, JH (2023)."The risk of dementia in multiple sclerosis and neuromyelitis optica spectrum disorder".Frontiers in Neuroscience.17:1214652.doi:10.3389/fnins.2023.1214652.PMC10309000.PMID37397465.
  54. ^Kanukollu, VM; Agarwal, P (8 January 2024),"Epiretinal Membrane",StatPearls,Treasure Island, Florida (FL): StatPearls Publishing,PMID32809538
  55. ^abTuifua, TS; Sood, AB; Abraham, JR; Srivastava, SK; Kaiser, PK; Sharma, S; Rachitskaya, A; Singh, RP; Reese, J; Ehlers, JP (December 2021)."Epiretinal Membrane Surgery Using Intraoperative OCT-Guided Membrane Removal in the DISCOVER Study versus Conventional Membrane Removal".Ophthalmology. Retina.5(12):1254–1262.doi:10.1016/j.oret.2021.02.013.PMC8390556.PMID33647472.
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