Статті в журналах: "Glomerular parietal epithelial cells"

1

Weinstein, T., R. Cameron, A. Katz, and M. Silverman. "Rat glomerular epithelial cells in culture express characteristics of parietal, not visceral, epithelium." Journal of the American Society of Nephrology 3, no. 6 (December 1992): 1279–87. http://dx.doi.org/10.1681/asn.v361279.

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Glomerular epithelial cells (GEC) in culture are derived from intact isolated glomeruli. Although there is general agreement about distinguishing GEC from mesangial and endothelial cells, there is still uncertainty regarding the visceral versus parietal origin of cultured GEC. If these cells are to provide a useful model system, it is necessary to establish well-defined cell populations. The purpose of this study was to evaluate this important issue by comparing the characteristics of cultured GEC with glomerular epithelium from rat kidney sections. By electron microscopy, GEC were polygonal, with cilia and desmosomes between cells, similar to parietal cells in situ. Because intermediate filaments are specifically expressed in differentiated cells in the kidney, the expression of intermediate filaments in cultured GEC were compared with those of intact glomeruli. Cultured GEC are positive for cytokeratin and negative for vimentin and desmin, identical to parietal cells in situ. In contrast, podocytes are positive for vimentin and desmin and negative for cytokeratin. In vivo, podocytes express gp330 and puromycin-aminonucleoside (PAN) susceptibility, which are used as markers for cultured GEC. Immunoperoxidase staining of rat kidney sections with monoclonal anti-gp330 demonstrated gp330 localization to the cell surface and coated pits of the parietal cells, similar to its localization in podocytes. The presence of gp330 in cultured GEC was confirmed by immunoblot. PAN administration to rats induced vacuolization and detachment from the basement membrane in the parietal cells of Bowman's capsule, similar to the cytotoxicity observed in podocytes.(ABSTRACT TRUNCATED AT 250 WORDS)

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2

Roeder, Sebastian S., Ania Stefanska, Diana G. Eng, Natalya Kaverina, Maria W. Sunseri, Bairbre A. McNicholas, Peter Rabinovitch, et al. "Changes in glomerular parietal epithelial cells in mouse kidneys with advanced age." American Journal of Physiology-Renal Physiology 309, no. 2 (July 15, 2015): F164—F178. http://dx.doi.org/10.1152/ajprenal.00144.2015.

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Kidney aging is accompanied by characteristic changes in the glomerulus, but little is known about the effect of aging on glomerular parietal epithelial cells (PECs), nor if the characteristic glomerular changes in humans and rats also occur in very old mice. Accordingly, a descriptive analysis was undertaken in 27-mo-old C57B6 mice, considered advanced age. PEC density was significantly lower in older mice compared with young mice (aged 3 mo), and the decrease was more pronounced in juxtamedullary glomeruli compared with outer cortical glomeruli. In addition to segmental and global glomerulosclerosis in older mice, staining for matrix proteins collagen type IV and heparan sulfate proteoglycan were markedly increased in Bowman's capsules of older mouse glomeruli, consistent with increased extracellular matrix production by PECs. De novo staining for CD44, a marker of activated and profibrotic PECs, was significantly increased in aged glomeruli. CD44 staining was more pronounced in the juxtamedullary region and colocalized with phosphorylated ERK. Additionally, a subset of aged PECs de novo expressed the epithelial-to-mesenchymal transition markers α-smooth muscle and vimentin, with no changes in epithelial-to-mesenchymal transition markers E-cadherin and β-catenin. The mural cell markers neural/glial antigen 2, PDGF receptor-β, and CD146 as well as Notch 3 were also substantially increased in aged PECs. These data show that mice can be used to better understand the aging kidney and that PECs undergo substantial changes, especially in juxtamedullary glomeruli, that may participate in the overall decline in glomerular structure and function with advancing age.

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3

Gharib, Sina A., Jeffrey W. Pippin, Takamoto Ohse, Scott G. Pickering, Ronald D. Krofft, and Stuart J. Shankland. "Transcriptional Landscape of Glomerular Parietal Epithelial Cells." PLoS ONE 9, no. 8 (August 15, 2014): e105289. http://dx.doi.org/10.1371/journal.pone.0105289.

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4

王, 金艳. "Parietal Epithelial Cells and Glomerular Dis-eases." Advances in Clinical Medicine 13, no. 04 (2023): 6478–88. http://dx.doi.org/10.12677/acm.2023.134909.

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5

Bianchi, C., J. Gutkowska, G. Thibault, R. Garcia, J. Genest, and M. Cantin. "Distinct localization of atrial natriuretic factor and angiotensin II binding sites in the glomerulus." American Journal of Physiology-Renal Physiology 251, no. 4 (October 1, 1986): F594—F602. http://dx.doi.org/10.1152/ajprenal.1986.251.4.f594.

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A comparative study of the localization of 125I-labeled atrial natriuretic factor (ANF) and 125I-labeled angiotensin II (ANG II) binding sites in the glomerulus of the rat, after an intravascular injection, has been done by ultrastructural radioautography. 125I-ANF binding sites are localized predominantly on the podocytes of the visceral epithelium (63%) followed by the endothelium of capillaries (14%), the parietal epithelium (13%), and finally mesangial cells (10%). In a comparative study, it was confirmed that 125I-ANG II uptake is localized predominantly on mesangial cells (60%) followed by epithelial visceral cells (23%) and the endothelium of capillaries (16%). Using isolated rat glomeruli, it was confirmed that ANG II decreases glomerular size (maximum effect of 15%) with an apparent half maximum effective concentration (EC50) between 10(-9) and 10(-8) M. Although ANF alone has no apparent effect on glomerular size, it inhibits the contractile effect of ANG II with a half maximum inhibitory concentration (IC50) between 10(-11) and 10(-10) M. These results suggest that an intraglomerular mechanism other than glomerular arteriolar resistance may be involved in the modulation of glomerular filtration rate by ANF. The presence of 125I-ANF uptake mainly in foot processes of visceral epithelial cells of glomeruli in vivo and the inhibition of ANG II decrease in glomerular size by ANF in vitro raise the possibility that ANF may regulate the ultrafiltration coefficient by two mechanisms: modulation of glomerular permeability, and surface area.

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6

Otani, Yuki, Osamu Ichii, Md Abdul Masum, Takashi Namba, Teppei Nakamura, and Yasuhiro Kon. "Castrated autoimmune glomerulonephritis mouse model shows attenuated glomerular sclerosis with altered parietal epithelial cell phenotype." Experimental Biology and Medicine 246, no. 11 (February 27, 2021): 1318–29. http://dx.doi.org/10.1177/1535370221996010.

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Sex hormones help in maintaining proper immunity as well as renal homeostasis in mammals, and these multi-functional properties characterize the onset of sex-dependent diseases. To clarify the contribution of sex hormones to autoimmune disease-related renal pathogenesis, BXSB/MpJ- Yaa was investigated as a murine autoimmune glomerulonephritis model. BXSB/MpJ- Yaa and its wild-type, BXSB/MpJ- Yaa+ were castrated or sham-operated at three weeks and examined until six months of age. Both castrated strains showed significantly lower serum testosterone levels and body weights than sham-operated mice. Castration did not change the disease phenotypes in BXSB/MpJ- Yaa+. At three months, both sham-operated and castrated BXSB/MpJ- Yaa manifested splenomegaly, autoantibody production, and glomerulonephritis, and castrated BXSB/MpJ- Yaa tended to show heavier spleen weights than the sham-operated group. At six months, both the treated BXSB/MpJ- Yaa showed equivalent autoimmune disease conditions; however, castrated mice clearly showed milder glomerular sclerotic lesions than the sham-operated groups. Urinary albumin excretion in castrated BXSB/MpJ- Yaa was significantly milder than in sham-operated mice at four months, but those of both the treated BXSB/MpJ- Yaa were comparable at six months. The examined renal histopathological indices in parietal epithelial cells were remarkably altered by castration. Briefly, castration decreased the height of parietal epithelial cells and total parietal epithelial cell number in BXSB/MpJ- Yaa at six months. For immunostaining, parietal epithelial cells facing the injured glomeruli of BXSB/MpJ- Yaa expressed CD44, an activated parietal epithelial cell marker, and CD44-positive parietal epithelial cells showed nuclear localization of the androgen receptor and proliferation marker Ki67. CD44- or Ki67-positive parietal epithelial cells were significantly fewer in castrated group than in sham-operated BXSB/MpJ- Yaa at six months. Further, quantitative indices for CD44-positive parietal epithelial cell number and frequency in renal corpuscles positively correlated with glomerular sclerotic severity in BXSB/MpJ- Yaa. In conclusion, androgen seemed to have an effect on both systemic immunity and renal morpho-function; however, the effect on the latter could be more clearly observed in BXSB/MpJ- Yaa, as parietal epithelial cell activation resulted in glomerular sclerosis.

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7

BARIÉTY, JEAN, PATRICK BRUNEVAL, GARY HILL, THEANO IRINOPOULOU, CHANTAL MANDET, and ALAIN MEYRIER. "Posttransplantation Relapse of FSGS Is Characterized by Glomerular Epithelial Cell Transdifferentiation." Journal of the American Society of Nephrology 12, no. 2 (February 2001): 261–74. http://dx.doi.org/10.1681/asn.v122261.

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Abstract. This study examined six cases of idiopathic nephrotic syndrome with primary lesions of focal segmental glomerulosclerosis (FSGS) that relapsed after renal transplantation. The glomerular lesions comprised the cellular, the collapsing, and the scar variants of FSGS and showed shedding of large round cells into Bowman's space and within the tubular lumens. Immunohistochemistry and confocal laser microscopy carried out on kidneys with FSGS relapse disclosed several phenomena. (1) Some podocytes that expressed podocalyxin, synaptopodin, and glomerular epithelial protein-1 were detached from the tuft and were free in the urinary space. (2) In the cellular variant, most podocytes had lost podocyte-specific epitopes (podocalyxin, synaptopodin, glomerular epithelial protein-1, Wilm's tumor protein-1, complement receptor-1, and vimentin). In the scar variant, these podocyte markers were absent from cobblestone-like epithelial cells and from pseudotubules. (3) Podocytes had acquired expression of various cytokeratins (CK; identified by the AE1/AE3, C2562, CK22, and AEL-KS2 monoclonal antibodies) that were not found in the podocytes of control glomeruli. Parietal epithelial cells expressed AE1/AE3 CK that were faintly, if ever, found on the parietal epithelial cells of normal glomeruli. (4) Numerous cells located at the periphery of the tuft or free in Bowman's space and within tubular lumens expressed macrophagic epitopes (identified by PGM1 [CD68], HAM56, and 25F9 monoclonal antibodies). These macrophage-like cells expressed the activation epitopes HLA-DR and CD16. (5) A number of these cells coexpressed podocalyxin + AE1/AE3 CK, podocalyxin + CD68, and CD68 + AE1/AE3. These findings suggest that in primary FSGS relapsing on transplanted kidneys, some “dysregulated” podocytes, occasionally some parietal epithelial cells, and possibly some tubular epithelial cells undergo a process of transdifferentiation. This process of transdifferentiation was especially striking in podocytes that acquired macrophagic and CK epitopes that are absent from normal adult and fetal podocytes.

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8

Appel, Daniel, David B. Kershaw, Bart Smeets, Gang Yuan, Astrid Fuss, Björn Frye, Marlies Elger, Wilhelm Kriz, Jürgen Floege, and Marcus J. Moeller. "Recruitment of Podocytes from Glomerular Parietal Epithelial Cells." Journal of the American Society of Nephrology 20, no. 2 (December 17, 2008): 333–43. http://dx.doi.org/10.1681/asn.2008070795.

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9

Smeets, Bart, and Marcus J. Moeller. "Parietal Epithelial Cells and Podocytes in Glomerular Diseases." Seminars in Nephrology 32, no. 4 (July 2012): 357–67. http://dx.doi.org/10.1016/j.semnephrol.2012.06.007.

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10

Kumar, R., J. Schaefer, J. P. Grande, and P. C. Roche. "Immunolocalization of calcitriol receptor, 24-hydroxylase cytochrome P-450, and calbindin D28k in human kidney." American Journal of Physiology-Renal Physiology 266, no. 3 (March 1, 1994): F477—F485. http://dx.doi.org/10.1152/ajprenal.1994.266.3.f477.

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The precise localization of the calcitriol (1 alpha,25-dihydroxyvitamin D3) receptor (VDR) and the 25-hydroxyvitamin D3 [25(OH)D3] 24-hydroxylase cytochrome P-450 in the human kidney is unknown. Using newly developed polyclonal antibodies against the human VDR, we demonstrate that the receptor is present in cells of the distal tubule, the collecting duct, the proximal tubule, and in the parietal epithelial cells of the glomerulus. In the distal tubule and collecting duct not all cells contain epitopes for the receptor. The protein is not detected in glomerular capillaries, in the glomerular mesangium, in the interstitium, or in blood vessels. Specific polyclonal antibodies directed against the 25(OH)D3 24-hydroxylase cytochrome P-450 demonstrate epitopes for the cytochrome in cells of the proximal tubule, the distal tubule, glomerular parietal epithelial cells, and mesangial cells. The protein is absent from interstitial cells. Calbindin D28k is present exclusively in principal cells of the distal tubule and collecting duct. In the human kidney, the VDR is present in cells where vitamin D-inducible proteins are found; conversely it is absent from cells where vitamin D-dependent proteins are not present.

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11

Yaoita, Eishin, and Yutaka Yoshida. "Polygonal epithelial cells in glomerular cell culture: Podocyte or parietal epithelial origin?" Microscopy Research and Technique 57, no. 4 (May 7, 2002): 212–16. http://dx.doi.org/10.1002/jemt.10075.

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12

Zhang, Jiong, Kim M. Hansen, Jeffrey W. Pippin, Alice M. Chang, Yoshinori Taniguchi, Ronald D. Krofft, Scott G. Pickering, Zhi-Hong Liu, Christine K. Abrass, and Stuart J. Shankland. "De novo expression of podocyte proteins in parietal epithelial cells in experimental aging nephropathy." American Journal of Physiology-Renal Physiology 302, no. 5 (March 1, 2012): F571—F580. http://dx.doi.org/10.1152/ajprenal.00516.2011.

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A progressive decrease in podocyte number underlies the development of glomerulosclerosis and reduced kidney function in aging nephropathy. Recent data suggest that under certain disease states, parietal epithelial cells (PECs) begin to express proteins considered specific to podocytes. To determine whether this phenomenon increases in aging kidneys, 4-, 12-, and 20-mo ad libitum-fed and 20-mo calorie-restricted (CR) rats were studied. Single and double immunostaining were performed with antibodies to the PEC protein paired box gene 2 (PAX2) and tight junction protein claudin-1, the podocyte-specific protein Wilms' tumor 1 (WT-1), and the proliferating cell protein (Ki-67). ImageJ software measured Bowman's basement membrane (BBM) length and glomerular tuft area in individual glomeruli from each animal to assess glomerular size. The results showed that in aged ad libitum rats, the decrease in number of podocytes/glomerular tuft area was accompanied by an increase in the number of PECs/BBM length at 12 and 20 mo ( P < 0.01 vs. 4 mo). The increase in PEC number was due to proliferation (increase in PAX2/Ki-67 double-positive cells). Aging was accompanied by a progressive increase in the number of glomerular cells double staining for PAX2 and WT-1. In contrast, the control 20-mo-old CR rats had no increase in glomerular size, and podocyte and PEC number were not altered. These results suggest that although the number of PECs and PECs expressing podocyte proteins increase in aging nephropathy, they are likely not sufficient to compensate for the decrease in podocyte number.

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13

Sakhi, Hamza, Anissa Moktefi, Khedidja Bouachi, Vincent Audard, Carole Hénique, Philippe Remy, Mario Ollero, and Khalil El Karoui. "Podocyte Injury in Lupus Nephritis." Journal of Clinical Medicine 8, no. 9 (August 29, 2019): 1340. http://dx.doi.org/10.3390/jcm8091340.

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Systemic lupus erythematosus (SLE) is characterized by a broad spectrum of renal lesions. In lupus glomerulonephritis, histological classifications are based on immune-complex (IC) deposits and hypercellularity lesions (mesangial and/or endocapillary) in the glomeruli. However, there is compelling evidence to suggest that glomerular epithelial cells, and podocytes in particular, are also involved in glomerular injury in patients with SLE. Podocytes now appear to be not only subject to collateral damage due to glomerular capillary lesions secondary to IC and inflammatory processes, but they are also a potential direct target in lupus nephritis. Improvements in our understanding of podocyte injury could improve the classification of lupus glomerulonephritis. Indeed, podocyte injury may be prominent in two major presentations: lupus podocytopathy and glomerular crescent formation, in which glomerular parietal epithelial cells play also a key role. We review here the contribution of podocyte impairment to different presentations of lupus nephritis, focusing on the podocyte signaling pathways involved in these lesions.

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Zoja, Carla, Pablo Bautista Garcia, Cinzia Rota, Sara Conti, Elena Gagliardini, Daniela Corna, Cristina Zanchi, et al. "Mesenchymal stem cell therapy promotes renal repair by limiting glomerular podocyte and progenitor cell dysfunction in adriamycin-induced nephropathy." American Journal of Physiology-Renal Physiology 303, no. 9 (November 1, 2012): F1370—F1381. http://dx.doi.org/10.1152/ajprenal.00057.2012.

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We previously reported that in a model of spontaneously progressive glomerular injury with early podocyte loss, abnormal migration, and proliferation of glomerular parietal epithelial progenitor cells contributed to the formation of synechiae and crescentic lesions. Here we first investigated whether a similar sequence of events could be extended to rats with adriamycin (ADR)-induced nephropathy. As a second aim, the regenerative potential of therapy with bone marrow-derived mesenchymal stem cells (MSCs) on glomerular resident cells was evaluated. In ADR-treated rats, decrease of WT1+ podocyte number due to apoptosis was associated with reduced glomerular expression of nephrin and CD2AP. As a consequence of podocyte injury, glomerular adhesions of the capillary tuft to the Bowman's capsule were observed, followed by crescent-like lesions and glomerulosclerosis. Cellular components of synechiae were either NCAM+ parietal progenitor cells or nestin+ podocytes. In ADR rats, repeated injections of MSCs limited podocyte loss and apoptosis and partially preserved nephrin and CD2AP. MSCs attenuated the formation of glomerular podocyte-parietal epithelial cell bridges and normalized the distribution of NCAM+ progenitor cells along the Bowman's capsule, thereby reducing glomerulosclerosis. Finding that MSCs increased glomerular VEGF expression and limited microvascular rarefaction may explain the prosurvival effect by stem cell therapy. MSCs also displayed anti-inflammatory activity. Coculture of MSCs with ADR-damaged podocytes showed a functional role of stem cell-derived VEGF on prosurvival pathways. These data suggest that MSCs by virtue of their tropism for damaged kidney and ability to provide a local prosurvival environment may represent a useful strategy to preserve podocyte viability and reduce glomerular inflammation and sclerosis.

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15

Shankland, Stuart J., Hans-Joachim Anders, and Paola Romagnani. "Glomerular parietal epithelial cells in kidney physiology, pathology, and repair." Current Opinion in Nephrology and Hypertension 22, no. 3 (May 2013): 302–9. http://dx.doi.org/10.1097/mnh.0b013e32835fefd4.

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16

Ohse, Takamoto, Alice M. Chang, Jeffrey W. Pippin, George Jarad, Kelly L. Hudkins, Charles E. Alpers, Jeffrey H. Miner, and Stuart J. Shankland. "A new function for parietal epithelial cells: a second glomerular barrier." American Journal of Physiology-Renal Physiology 297, no. 6 (December 2009): F1566—F1574. http://dx.doi.org/10.1152/ajprenal.00214.2009.

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The functional role of glomerular parietal epithelial cells (PECs) remains poorly understood. To test the hypothesis that PECs form an impermeable barrier to filtered protein through the formation of tight junctions (TJ), studies were performed in normal animals and in the anti-glomerular basement membrane (GBM) model of crescentic nephritis. Electron microscopy showed well-defined TJ between PECs in normal mice, which no longer could be identified when these cells became extensively damaged or detached from their underlying Bowman's basement membrane. The TJ proteins claudin-1, zonula occludens-1, and occludin stained positive in PECs; however, staining decreased in anti-GBM disease. To show that these events were associated with increased permeability across the PEC-Bowman's basement membrane barrier, control and diseased animals were injected intravenously with either Texas red-conjugated dextran (3 kDa) or ovalbumin (45 kDa) tracers. As expected, both tracers were readily filtered across the glomerular filtration barrier and taken up by proximal tubular cells. However, when the glomerular filtration barrier was injured in anti-GBM disease, tracers were taken up by podocytes and PECs. Moreover, tracers were also detected between PECs and the underlying Bowman's basement membrane, and in many instances were detected in the extraglomerular space. We propose that together with its underlying Bowman's basement membrane, the TJ of PECs serve as a second barrier to protein. When disturbed following PEC injury, the increase in permeability of this layer to filtered protein is a mechanism underlying periglomerular inflammation characteristic of anti-GBM disease.

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17

SHIRATO, ISAO, KATSUHIKO ASANUMA, YUKIHIKO TAKEDA, KAYO HAYASHI, and YASUHIKO TOMINO. "Protein Gene Product 9.5 Is Selectively Localized in Parietal Epithelial Cells of Bowman's Capsule in the Rat Kidney." Journal of the American Society of Nephrology 11, no. 12 (December 2000): 2381–86. http://dx.doi.org/10.1681/asn.v11122381.

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Abstract. Parietal epithelial cells (PEC) of Bowman's capsules cover the inner aspect of Bowman's capsules and are believed to contribute to extracapillary lesions of glomerulonephritis such as crescent formation. In glomerular research including cell culture experiments and pathology, differentiation between PEC and podocytes has frequently been a major problem. Immunohistochemistry of the adult rat kidney for protein gene product 9.5 (PGP 9.5), a neuron-specific ubiquitin C-terminal hydrolase, demonstrated selective localization of the immunoreactivity in PEC. At the urinary pole of the glomerulus, immunoreactive PEC were clearly differentiated from proximal tubular cells that were negative for PGP 9.5. In the subcapsular nephrogenic zone of newborn rat kidney, immunoreactivity was observed in almost all cells in the commashaped body and early S-shaped body and selectively in PEC in the late S-shaped body and capillary-stage glomerulus. In rat glomerular disease models (Masugi-nephritis and puromycin aminonucleoside nephrosis), cells that consisted of cellular crescents or adhered to glomerular tufts were positive for PGP 9.5. The selective localization of PGP 9.5 in PEC in rat kidney provides a new cytochemical marker for identifying the cells. Development expression of the protein suggests that PGP 9.5 is involved in the processes of nephrogenesis of rat kidney.

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18

Ohse, Takamoto, Michael R. Vaughan, Jeffrey B. Kopp, Ronald D. Krofft, Caroline B. Marshall, Alice M. Chang, Kelly L. Hudkins, Charles E. Alpers, Jeffrey W. Pippin, and Stuart J. Shankland. "De novo expression of podocyte proteins in parietal epithelial cells during experimental glomerular disease." American Journal of Physiology-Renal Physiology 298, no. 3 (March 2010): F702—F711. http://dx.doi.org/10.1152/ajprenal.00428.2009.

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Studies have shown that certain cells of the glomerular tuft begin to express proteins considered unique to other cell types upon injury. Little is known about the response of parietal epithelial cells (PEC) to injury. To determine whether PECs change their phenotype upon injury to also express proteins traditionally considered podocyte specific, the following four models of glomerular disease were studied: the transforming growth factor (TGF)-β1 transgenic mouse model of global glomerulosclerosis, the adriamycin model of focal segmental glomerulosclerosis (FSGS), the anti-glomerular basement membrane (GBM) model of crescentic glomerulonephritis, and the passive Heymann nephritis model of membranous nephropathy. Double immunostaining was performed with antibodies to podocyte-specific proteins (synaptopodin and Wilms' tumor 1) and antibodies to PEC specific proteins (paired box gene 8 and claudin-1). No double staining was detected in normal mice. In contrast, the results showed a statistical increase in the number of cells attached to Bowman basement membrane that were double-positive for both podocyte/PEC proteins in TGF-β;1 transgenic, anti-GBM, and membranous animals. Double-positive cells for both podocyte and PEC proteins were also statistically increased in the glomerular tuft in TGF-β1 transgenic, anti-GBM, and FSGS mice. These results are consistent with glomerular cells coexpressing podocyte and PEC proteins in experimental glomerular disease, but not under normal circumstances.

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Ye, Chen, Wei Xiong, Chun-Tao Lei, Hui Tang, Hua Su, Fan Yi, and Chun Zhang. "MAD2B contributes to parietal epithelial cell activation and crescentic glomerulonephritis via Skp2." American Journal of Physiology-Renal Physiology 319, no. 4 (October 1, 2020): F636—F646. http://dx.doi.org/10.1152/ajprenal.00216.2020.

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Mitotic spindle assembly checkpoint protein 2 (MAD2B), a well-known anaphase-promoting complex/cyclosome (APC/C) inhibitor and a small subunit of DNA polymerase-ζ, is critical for mitotic control and DNA repair. Previously, we detected a strong increase of MAD2B in the glomeruli from patients with crescentic glomerulonephritis and anti-glomerular basement membrane (anti-GBM) rats, which predominantly originated from activated parietal epithelial cells (PECs). Consistently, in vitro MAD2B was increased in TNF-α-treated PECs, along with cell activation and proliferation, as well as extracellular matrix accumulation, which could be reversed by MAD2B genetic depletion. Furthermore, we found that expression of S phase kinase-associated protein 2 (Skp2), an APC/CCDH1 substrate, was increased in the glomeruli of anti-GBM rats, and TNF-α-stimulated PECs and could be suppressed by MAD2B depletion. Additionally, genetic deletion of Skp2 inhibited TNF-α-induced PEC activation and dysfunction. Finally, TNF-α blockade or glucocorticoid therapy administered to anti-GBM rats could ameliorate MAD2B and Skp2 accumulation as well as weaken PEC activation. Collectively, our data suggest that MAD2B has a pivotal role in the pathogenesis of glomerular PEC activation and crescent formation through induction of Skp2 expression.

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Ohse, Takamoto, Jeffrey W. Pippin, Michael R. Vaughan, Paul T. Brinkkoetter, Ronald D. Krofft, and Stuart J. Shankland. "Establishment of Conditionally Immortalized Mouse Glomerular Parietal Epithelial Cells in Culture." Journal of the American Society of Nephrology 19, no. 10 (July 2, 2008): 1879–90. http://dx.doi.org/10.1681/asn.2007101087.

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21

Smeets, Bart, Sandra Uhlig, Astrid Fuss, Fieke Mooren, Jack F. M. Wetzels, Jürgen Floege, and Marcus J. Moeller. "Tracing the Origin of Glomerular Extracapillary Lesions from Parietal Epithelial Cells." Journal of the American Society of Nephrology 20, no. 12 (November 16, 2009): 2604–15. http://dx.doi.org/10.1681/asn.2009010122.

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22

Lazareth, Hélène, Olivia Lenoir, and Pierre-Louis Tharaux. "Parietal epithelial cells role in repair versus scarring after glomerular injury." Current Opinion in Nephrology and Hypertension 29, no. 3 (May 2020): 293–301. http://dx.doi.org/10.1097/mnh.0000000000000600.

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23

Zhong, Jianyong, Jacob B. Whitman, Hai-Chun Yang, and Agnes B. Fogo. "Mechanisms of Scarring in Focal Segmental Glomerulosclerosis." Journal of Histochemistry & Cytochemistry 67, no. 9 (May 22, 2019): 623–32. http://dx.doi.org/10.1369/0022155419850170.

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Focal segmental glomerulosclerosis (FSGS) presents with scar in parts of some glomeruli and often progresses to global and diffuse glomerulosclerosis. Podocyte injury is the initial target in primary FSGS, induced by a circulating factor. Several gene variants, for example, APOL1, are associated with increased susceptibility to FSGS. Primary FSGS may be due to genetic mutation in key podocyte genes. Increased work stress after loss of nephrons, epigenetic mechanisms, and various profibrotic pathways can contribute to progressive sclerosis, regardless of the initial injury. The progression of FSGS lesions also involves crosstalk between podocytes and other kidney cells, such as parietal epithelial cells, glomerular endothelial cells, and even tubular epithelial cells. New insights related to these mechanisms could potentially lead to new therapeutic strategies to prevent progression of FSGS.

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Zhang, Jiong, Jeffrey W. Pippin, Ronald D. Krofft, Shokichi Naito, Zhi-Hong Liu, and Stuart J. Shankland. "Podocyte repopulation by renal progenitor cells following glucocorticoids treatment in experimental FSGS." American Journal of Physiology-Renal Physiology 304, no. 11 (June 1, 2013): F1375—F1389. http://dx.doi.org/10.1152/ajprenal.00020.2013.

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Prednisone is a mainstay of treatment for patients with focal segmental glomerulosclerosis (FSGS), a disease characterized by reduced podocyte number and glomerulosclerosis. Although the systemic immune-modulatory effects of prednisone are well-known, direct tissue effects on glomerular cells are poorly understood. Experimental FSGS was induced in mice with a cytotoxic anti-podocyte antibody, resulting in an abrupt decrease in podocyte number by day 3, proteinuria, and the development of glomerulosclerosis. Administering daily prednisone to mice with FSGS, beginning at day 3, significantly increased podocyte number at weeks 2 and 4. Podocyte number did not increase in control mice with FSGS given DMSO. The increase in podocyte number in prednisone-treated mice correlated significantly with reduced glomerulosclerosis. Prednisone reduced podocyte apoptosis measured by synaptopodin+/caspase-3+ double staining. Additionally, the number of podocyte progenitors, defined as cells expressing both a parietal epithelial cell protein and a podocyte protein, was significantly increased in prednisone-treated mice with FSGS at weeks 2 and 4. This was associated with increased phospho-ERK staining in both parietal epithelial cells (PAX2+/p-ERK+) and in podocyte progenitors (WT-1+/p-ERK+ lining Bowman's capsule). These data show that in this model of experimental FSGS, prednisone augments glomerular repair by increasing podocyte number through direct effects on both glomerular epithelial cells. Prednisone limits podocyte loss by reducing apoptosis, and it increases regeneration by augmenting the number of podocyte progenitors. The data support a direct glomerular cell action for prednisone in improving outcomes in FSGS.

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25

Wang, Jiayi, Jianyong Zhong, Hai-Chun Yang, and Agnes B. Fogo. "Cross Talk from Tubules to Glomeruli." Toxicologic Pathology 46, no. 8 (August 29, 2018): 944–48. http://dx.doi.org/10.1177/0192623318796784.

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Tubular injury sensitizes glomeruli to injury. We review potential mechanisms of this tubuloglomerular cross talk. In the same nephron, tubular injury can cause stenosis of the glomerulotubular junction and finally result in atubular glomeruli. Tubular injury also affects glomerular filtration function through tubuloglomerular feedback. Progenitor cells, that is, parietal epithelial cells and renin positive cells, can be involved in repair of injured glomeruli and also may be modulated by tubular injury. Loss of nephrons induces additional workload and stress on remaining nephrons. Hypoxia and activation of the renin–angiotensin–aldosterone system induced by tubular injury also modulate tubuloglomerular cross talk. Therefore, effective therapies in chronic kidney disease may need to aim to interrupt this deleterious tubuloglomerular cross talk.

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26

Nadasdy, T., Z. Laszik, K. E. Blick, L. D. Johnson, and F. G. Silva. "Proliferative activity of intrinsic cell populations in the normal human kidney." Journal of the American Society of Nephrology 4, no. 12 (June 1994): 2032–39. http://dx.doi.org/10.1681/asn.v4122032.

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The proliferative activity of various normal human renal cell populations is unknown. Recently, antibodies to cell proliferation-associated nuclear proteins, such as proliferating cell nuclear antigen (PCNA) and KI-67, which are applicable to archival paraffin sections, became available. With antibodies to PCNA and Ki-67 after microwave pretreatment of the paraffin sections, the proliferation indexes (ratio of positive nuclei with PCNA and Ki-67 antibodies/all nuclei counted x 100, i.e. percentage of positive cells) of 12 different intrinsic renal cell populations in 20 normal human kidneys have been determined. The following proliferation indexes (percentages of positive cells) were found with the PCNA and the Ki-67 antibodies, respectively: proximal tubular epithelium, 0.22, 0.24; thin limb of Henle, 0.29, 0.30; thick ascending limb of Henle, 0.32, 0.29; distal tubular epithelium (distal convoluted tubules and cortical collecting ducts, 0.33, 0.44; medullary collecting ducts, 0.32, 0.3; glomerular mesangial cells, 0.07, 0.12; glomerular visceral epithelial cells, 0.04, 0.08; glomerular parietal epithelial cells, 0.07, 0.1; glomerular capillary endothelium, 0.42, 0.47; peritubular capillary endothelial cells, 0.38, 0.43; endothelium of large intrarenal vessels (arteries and veins), 0.09, 0.12. Thus, normally capillary endothelium (glomerular and peritubular) appears to have the highest proliferation index in the human kidney by these techniques. These results indicate major variation in the proliferative activity of normal human renal cell populations, along with a significant correlation between PCNA and Ki-67 staining. Furthermore, this study provides normal values for the proliferative activity of different human renal cell populations.(ABSTRACT TRUNCATED AT 250 WORDS)

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27

Kabgani, Nazanin, Tamara Grigoleit, Kevin Schulte, Antonio Sechi, Sibille Sauer-Lehnen, Carmen Tag, Peter Boor, et al. "Primary Cultures of Glomerular Parietal Epithelial Cells or Podocytes with Proven Origin." PLoS ONE 7, no. 4 (April 18, 2012): e34907. http://dx.doi.org/10.1371/journal.pone.0034907.

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28

Su, Hua, Shan Chen, Fang-Fang He, Yu-Mei Wang, Philip Bondzie, and Chun Zhang. "New Insights into Glomerular Parietal Epithelial Cell Activation and Its Signaling Pathways in Glomerular Diseases." BioMed Research International 2015 (2015): 1–8. http://dx.doi.org/10.1155/2015/318935.

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The glomerular parietal epithelial cells (PECs) have aroused an increasing attention recently. The proliferation of PECs is the main feature of crescentic glomerulonephritis; besides that, in the past decade, PEC activation has been identified in several types of noninflammatory glomerulonephropathies, such as focal segmental glomerulosclerosis, diabetic glomerulopathy, and membranous nephropathy. The pathogenesis of PEC activation is poorly understood; however, a few studies delicately elucidate the potential mechanisms and signaling pathways implicated in these processes. In this review we will focus on the latest observations and concepts about PEC activation in glomerular diseases and the newest identified signaling pathways in PEC activation.

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29

KONDO, DAISUKE, TADASHI YAMAMOTO, EISHIN YAOITA, PATRIA E. DANIELSON, HIDEYUKI KOBAYASHI, KAZUFUMI OHSHIRO, HARUKO FUNAKI, et al. "Localization of Olfactomedin-Related Glycoprotein Isoform (BMZ) in the Golgi Apparatus of Glomerular Podocytes in Rat Kidneys." Journal of the American Society of Nephrology 11, no. 5 (May 2000): 803–13. http://dx.doi.org/10.1681/asn.v115803.

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Abstract. A gene encoding olfactomedin-related glycoprotein was isolated from rat glomerulus despite its prior identification as a neuron-specific gene. The mRNA expression was remarkably intense in renal glomerulus and brain and faint in the lung and eye among rat systemic organs. Although the brain contained four mRNA variants (AMY, AMZ, BMY, and BMZ) transcribed from a single gene, the glomerulus, lung, and eye expressed only two variants (BMZ and BMY). The glycoprotein was intensely immunolocalized in glomerular podocytes and neurons by using an antibody against synthetic peptide of the M region, but weak in endothelial cells of the kidney and lung. Bronchiolar epithelial cells in the lung, and ciliary, corneal, and iris epithelial cells in the eye were also stained. Immunogold electron microscopy revealed selective localization of olfactomedin-related glycoprotein at the Golgi apparatus in podocytes. In glomerular culture, the staining was also intense at a juxtanuclear region in synaptopodin-positive epithelial cells of irregular shape (phenotypic feature of podocytes), whereas it was weak in synaptopodin-negative ones of cobblestone-like appearance (phenotypic feature of parietal epithelial cells of Bowman's capsule). Interestingly, Western blot analysis identified an intense band corresponding to BMZ isoform and another faint band corresponding to BMY isoform in the glomerulus, whereas the intensity of these two bands were nearly equal in the lung and eye. In the brain, four bands corresponding to four isoforms were observed apparently. Computer sequence analysis predicted coiled-coil structures in the secondary structure of the glycoprotein similar to those in Golgi autoantigens, suggesting significant roles in the unique functions of the Golgi apparatus in rat podocytes and neurons.

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30

Zhang, Jiong, Jeffrey W. Pippin, Michael R. Vaughan, Ronald D. Krofft, Yoshinori Taniguchi, Paola Romagnani, Peter J. Nelson, Zhi-Hong Liu, and Stuart J. Shankland. "Retinoids Augment the Expression of Podocyte Proteins by Glomerular Parietal Epithelial Cells in Experimental Glomerular Disease." Nephron Experimental Nephrology 121, no. 1-2 (2012): e23-e37. http://dx.doi.org/10.1159/000342808.

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31

HIR, MICHEL LE, CORNELIA KELLER, VALÉRIE ESCHMANN, BRUNHILDE HÄHNEL, HILTRAUDE HOSSER, and WILHELM KRIZ. "Podocyte Bridges between the Tuft and Bowman's Capsule: An Early Event in Experimental Crescentic Glomerulonephritis." Journal of the American Society of Nephrology 12, no. 10 (October 2001): 2060–71. http://dx.doi.org/10.1681/asn.v12102060.

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Abstract. Although experimental crescentic glomerulonephritis starts with an endocapillary inflammation, the crescents themselves seem to originate from the proliferation of parietal epithelial cells (PEC). In this study, an attempt was made to disclose a link between the two processes by a morphologic analysis of early stages of the disease. Mice were immunized with rabbit IgG in complete Freund's adjuvant on day -6. At day 0, they received an intravenous injection of a rabbit antiglomerular basement membrane serum. On days 3, 6, and 10, the kidneys were fixed by vascular perfusion for examination by light and electron microscopy. On day 3, morphologic alterations affected mainly the endocapillary compartment; most podocytes appeared to be intact. On day 6, alterations of podocytes were widespread, including foot process effacement and prominent microvillous transformation, and some crescents were found. On day 10, crescents were found in 40% of glomeruli. The most surprising finding was podocytes that adhered to both the glomerular basement membrane and the parietal basement membrane, thus forming bridges between the tuft and Bowman's capsule. Those podocyte bridges were sparse on day 3 but were regularly encountered on days 6 and 10 in glomeruli without crescents and also as a component of crescents. They were interposed between PEC and later between the cells of a crescent without formation of junctional connection with these cells. It is proposed that the spreading of podocytes on the parietal basement membrane represents a lesion of the parietal epithelium and that this process initiates the proliferation of PEC to form a crescent.

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32

Burnworth, Bettina, Jeff Pippin, Prasanthi Karna, Shin Akakura, Ron Krofft, Guoqiang Zhang, Kelly Hudkins, et al. "SSeCKS sequesters cyclin D1 in glomerular parietal epithelial cells and influences proliferative injury in the glomerulus." Laboratory Investigation 92, no. 4 (January 16, 2012): 499–510. http://dx.doi.org/10.1038/labinvest.2011.199.

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33

Bharati, Joyita, Praveen N. Chander, and Pravin C. Singhal. "Parietal Epithelial Cell Behavior and Its Modulation by microRNA-193a." Biomolecules 13, no. 2 (January 31, 2023): 266. http://dx.doi.org/10.3390/biom13020266.

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Glomerular parietal epithelial cells (PECs) have been increasingly recognized to have crucial functions. Lineage tracking in animal models showed the expression of a podocyte phenotype by PECs during normal glomerular growth and after acute podocyte injury, suggesting a reparative role of PECs. Conversely, activated PECs are speculated to be pathogenic and comprise extracapillary proliferation in focal segmental glomerulosclerosis (FSGS) and crescentic glomerulonephritis (CrescGN). The reparative and pathogenic roles of PECs seem to represent two sides of PEC behavior directed by the local milieu and mediators. Recent studies suggest microRNA-193a (miR193a) is involved in the pathogenesis of FSGS and CrescGN. In a mouse model of primary FSGS, the induction of miR193a caused the downregulation of Wilms’ tumor protein, leading to the dedifferentiation of podocytes. On the other hand, the inhibition of miR193a resulted in reduced crescent lesions in a mouse model of CrescGN. Interestingly, in vitro studies report that the downregulation of miR193a induces trans-differentiation of PECs into a podocyte phenotype. This narrative review highlights the critical role of PEC behavior in health and during disease and its modulation by miR193a.

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34

Goto, S., E. Yaoita, H. Matsunami, D. Kondo, T. Yamamoto, K. Kawasaki, M. Arakawa, and I. Kihara. "Involvement of R-cadherin in the early stage of glomerulogenesis." Journal of the American Society of Nephrology 9, no. 7 (July 1998): 1234–41. http://dx.doi.org/10.1681/asn.v971234.

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The earliest commitment to the formation of glomeruli is recognizable in S-shaped bodies. Although cell-cell adhesion seems likely to play a crucial role in this process, how glomerular epithelial cells segregate from the other parts of the nephron is unknown. In this study, immunofluorescence microscopy and monoclonal antibodies specific for mouse R-, E-, P- and N-cadherins were used to examine which of these adhesion molecules are involved in glomerulogenesis of the mouse kidney. Weak R-cadherin staining was first found in the vesicle stage, becoming restricted to glomerular visceral epithelial cells (VEC) during the S-shaped body stage. The intensity of this staining became stronger in the capillary loop stage, whereas parietal epithelial cells (PEC) and tubular cells did not stain. In the maturing stage, VEC gradually lost their staining for R-cadherin. E-cadherin was detected in ureteric buds and the upper limb of S-shaped bodies. From the capillary loop to the maturing stage, anti-E-cadherin stained epithelial cells in all tubule segments, but no label was seen in VEC or PEC. P-cadherin was also stained in the ureteric buds and in the upper limb of S-shaped bodies. N-Cadherin was weakly stained in cells at the vesicle stage, but thereafter staining of N-cadherin was not detected at any stage of glomerular formation. Immunoelectron microscopy of differentiating VEC was performed using antibodies specific to alpha-catenin, which is associated with cadherin. Subsequently, immunogold particles identifying alpha-catenin were localized on junctions between primary processes of VEC. These findings indicate that R-cadherin is uniquely expressed in differentiating VEC, suggesting an important role in the early stages of glomerulogenesis.

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35

Kamata, Mariko, Kanako Hosono, Kou Hatanaka, Yoshiya Ito, Stuart J. Shankland, and Hideki Amano. "Sex differences in podocytes and glomerular parietal epithelial cells in aging mice kidney." Proceedings for Annual Meeting of The Japanese Pharmacological Society 97 (2023): 2—B—O08–3. http://dx.doi.org/10.1254/jpssuppl.97.0_2-b-o08-3.

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36

Choi, Jae-Youn, Sun-Ah Nam, and Jung-Ho Cha. "Invasion of Calponin-positive Glomerular Parietal Epithelial Cells into Glomerular Tuft Is Related to the Development of Glomerulosclerosis." Applied Microscopy 44, no. 4 (December 30, 2014): 117–22. http://dx.doi.org/10.9729/am.2014.44.4.117.

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37

Pippin, Jeffrey W., Matthew A. Sparks, Sean T. Glenn, Sandra Buitrago, Thomas M. Coffman, Jeremy S. Duffield, Kenneth W. Gross, and Stuart J. Shankland. "Cells of Renin Lineage Are Progenitors of Podocytes and Parietal Epithelial Cells in Experimental Glomerular Disease." American Journal of Pathology 183, no. 2 (August 2013): 542–57. http://dx.doi.org/10.1016/j.ajpath.2013.04.024.

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38

Okamoto, Takayuki, Satoshi Sasaki, Takeshi Yamazaki, Yasuyuki Sato, Hironobu Ito, and Tadashi Ariga. "Prevalence of CD44-Positive Glomerular Parietal Epithelial Cells Reflects Podocyte Injury in Adriamycin Nephropathy." Nephron Experimental Nephrology 124, no. 3-4 (January 8, 2014): 11–18. http://dx.doi.org/10.1159/000357356.

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39

Roeder, Sebastian S., Taylor J. Barnes, Jonathan S. Lee, India Kato, Diana G. Eng, Natalya V. Kaverina, Maria W. Sunseri, et al. "Activated ERK1/2 increases CD44 in glomerular parietal epithelial cells leading to matrix expansion." Kidney International 91, no. 4 (April 2017): 896–913. http://dx.doi.org/10.1016/j.kint.2016.10.015.

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40

Eng, Diana G., Maria W. Sunseri, Natalya V. Kaverina, Sebastian S. Roeder, Jeffrey W. Pippin, and Stuart J. Shankland. "Glomerular parietal epithelial cells contribute to adult podocyte regeneration in experimental focal segmental glomerulosclerosis." Kidney International 88, no. 5 (November 2015): 999–1012. http://dx.doi.org/10.1038/ki.2015.152.

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41

Zeng, Yeting, Xinrui Wang, Feilai Xie, and Zhiyong zheng. "Ischemia-induced glomerular parietal epithelial cells hyperplasia: Commonly misdiagnosed cellular crescent in renal biopsy." Pathology - Research and Practice 213, no. 8 (August 2017): 982–86. http://dx.doi.org/10.1016/j.prp.2017.04.006.

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42

Ito, Yasuhiko, Roel Goldschmeding, Hirotake Kasuga, Nike Claessen, Masahiro Nakayama, Yukio Yuzawa, Akiho Sawai, Seiichi Matsuo, Jan J. Weening та Jan Aten. "Expression patterns of connective tissue growth factor and of TGF-β isoforms during glomerular injury recapitulate glomerulogenesis". American Journal of Physiology-Renal Physiology 299, № 3 (вересень 2010): F545—F558. http://dx.doi.org/10.1152/ajprenal.00120.2009.

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Transforming growth factor (TGF)-β1, -β2, and -β3 are involved in control of wound repair and development of fibrosis. Connective tissue growth factor (CTGF) expression is stimulated by all TGF-β isoforms and is abundant in glomerulosclerosis and other fibrotic disorders. CTGF is hypothesized to mediate profibrotic effects of TGF-β1 or to facilitate interaction of TGF-β1 with its receptor, but its interactions with TGF-β isoforms in nonpathological conditions are unexplored so far. Tissue repair and remodeling may recapitulate gene transcription at play in organogenesis. To further delineate the relationship between CTGF and TGF-β, we compared expression patterns of CTGF and TGF-β isoforms in rat and human glomerulogenesis and in various human glomerulopathies. CTGF mRNA was present in the immediate precursors of glomerular visceral and parietal epithelial cells in the comma- and S-shaped stages, but not in earlier stages of nephron development. During the capillary loop and maturing glomerular stages and simultaneous with the presence of TGF-β1, -β2, and -β3 protein, CTGF mRNA expression was maximal and present only in differentiating glomerular epithelial cells. CTGF protein was also present on precursors of mesangium and glomerular endothelium, suggesting possible paracrine interaction. Concomitant with the presence of TGF-β2 and -β3 protein, and in the absence of TGF-β1, CTGF mRNA and protein expression was restricted to podocytes in normal adult glomeruli. However, TGF-β1 and CTGF were again coexpressed, often with TGF-β2 and -β3, in particular in podocytes in proliferative glomerulonephritis and also in mesangial cells in diabetic nephropathy and IgA nephropathy (IgA NP). Coordinated expression of TGF-β isoforms and of CTGF may be involved in normal glomerulogenesis and possibly in maintenance of glomerular structure and function at adult age. Prolonged overexpression of TGF-β1 and CTGF is associated with development of severe glomerulonephritis and glomerulosclerosis.

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43

Frelier, P. F., D. L. Armstrong, and J. Pritchard. "Ovine Mesangiocapillary Glomerulonephritis Type I and Crescent Formation." Veterinary Pathology 27, no. 1 (January 1990): 26–34. http://dx.doi.org/10.1177/030098589002700104.

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Morphologic examination of four Finnish Landrace mixed-breed lambs, 27 to 35 days of age, affected with mesangiocapillary glomerulonephritis type 1, demonstrated a progressive glomerulonephritis. By 27 days of age, three lambs had crescents in 58 to 93% of glomeruli. These three lambs were also uremic. The accelerated rate of crescent formation was attributed to infiltrating polymorphonuclear leukocytes and monocytes, the result of discontinuities (gaps) in the glomerular basement membrane, and to the loss of the integrity of Bowman's capsule. In the three lambs, platelets were identified adjacent to the endothelium or denuded glomerular basement membrane. Two distinctly different types of crescents were noted, apparently dependent on the integrity of Bowman's capsule. One type resulted from the influx of inflammatory cells and dissociation of parietal epithelial cells from Bowman's capsule. The other type was more extensive and contained collagen and was associated with damage to Bowman's capsule resulting in cellular infiltration from the interstitium and sclerosis. Based on morphologic similarities, ovine mesangiocapillary glomerulonephritis is a suitable model for studying the pathogenesis and treatment of mesangiocapillary glomerulonephritis type 1 in human beings.

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Hayashi, Asako, Takayuki Okamoto, Takeshi Yamazaki, Yasuyuki Sato, Toshiyuki Takahashi, and Tadashi Ariga. "CD44-Positive Glomerular Parietal Epithelial Cells in a Mouse Model of Calcineurin Inhibitors-Induced Nephrotoxicity." Nephron 142, no. 1 (2019): 71–81. http://dx.doi.org/10.1159/000497325.

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45

Hamatani, Hiroko, Keiju Hiromura, Toru Sakairi, Satoshi Takahashi, Mitsuharu Watanabe, Akito Maeshima, Takamoto Ohse, Jeffery W. Pippin, Stuart J. Shankland, and Yoshihisa Nojima. "Expression of a novel stress-inducible protein, sestrin 2, in rat glomerular parietal epithelial cells." American Journal of Physiology-Renal Physiology 307, no. 6 (September 15, 2014): F708—F717. http://dx.doi.org/10.1152/ajprenal.00625.2013.

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Sestrin 2, initially identified as a p53 target protein, accumulates in cells exposed to stress and inhibits mammalian target of rapamycin (mTOR) signaling. In normal rat kidneys, sestrin 2 was selectively expressed in parietal epithelial cells (PECs), identified by the marker protein gene product 9.5. In adriamycin nephropathy, sestrin 2 expression decreased in PECs on day 14, together with increased expression of phosphorylated S6 ribosomal protein (P-S6RP), a downstream target of mTOR. Sestrin 2 expression was markedly decreased on day 42, coinciding with glomerulosclerosis and severe periglomerular fibrosis. In puromycin aminonucleoside nephropathy, decreased sestrin 2 expression, increased P-S6RP expression, and periglomerular fibrosis were observed on day 9, when massive proteinuria developed. These changes were transient and nearly normalized by day 28. In crescentic glomerulonephritis, sestrin 2 expression was not detected in cellular crescents, whereas P-S6RP increased. In conditionally immortalized cultured PECs, the forced downregulation of sestrin 2 by short hairpin RNA resulted in increased expression of P-S6RP and increased apoptosis. These data suggest that sestrin 2 is involved in PEC homeostasis by regulating the activity of mTOR. In addition, sestrin 2 could be a novel marker of PECs, and decreased expression of sestrin 2 might be a marker of PEC injury.

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46

Yang, Haichun, Jianyong Zhong, Shilin Zhao, Angela R. Kruse, Morad C. Malek, Jeffrey M. Spraggins, and Agnes B. Fogo. "Spatial Transcriptomic Analysis Reveals Altered Gene Expression in Glomerular Parietal Epithelial Cells Following Tubular Injury." Journal of the American Society of Nephrology 34, no. 11S (November 2023): 315. http://dx.doi.org/10.1681/asn.20233411s1315c.

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47

Suzuki, Taihei, Diana G. Eng, Aaron D. McClelland, Jeffrey W. Pippin, and Stuart J. Shankland. "Cells of NG2 lineage increase in glomeruli of mice following podocyte depletion." American Journal of Physiology-Renal Physiology 315, no. 5 (November 1, 2018): F1449—F1464. http://dx.doi.org/10.1152/ajprenal.00118.2018.

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Under certain circumstances, podocytes can be partially replaced following their loss in disease. The inability of podocytes to proliferate suggests that replacement derives from other cell types. Because neural/glial antigen 2 (NG2)-expressing cells can serve as progenitors in other organs and because herein we showed increased NG2 staining in podocytes following their loss in experimental focal segmental glomerulosclerosis, we used lineage tracing in NG2-CreER tdTomato mice to test the hypothesis that partial podocyte replacement might derive from this cell population. The percentage of glomeruli with red fluorescence protein (RFP)-labeled NG2 cells increased following podocyte depletion, which was augmented by enalapril. However, BrdU was not detected in RFP-labeled cells, consistent with the migration of these cells to the glomerulus. Within glomeruli, RFP-labeled cells did not coexpress podocyte proteins (p57, synaptopodin, nephrin, or podocin) but did coexpress markers for mesangial (α8 integrin, PDGFβ receptor) and parietal epithelial cells (PAX8, src-suppressed C-kinase substrate). These results suggest that following podocyte depletion, cells of NG2 lineage do not serve as adult podocyte progenitors but have the ability to transdifferentiate to mesangial and parietal epithelial cell fates.

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48

Forbes, Michael S., Barbara A. Thornhill, and Robert L. Chevalier. "Proximal tubular injury and rapid formation of atubular glomeruli in mice with unilateral ureteral obstruction: a new look at an old model." American Journal of Physiology-Renal Physiology 301, no. 1 (July 2011): F110—F117. http://dx.doi.org/10.1152/ajprenal.00022.2011.

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Unilateral ureteral obstruction (UUO), employed extensively as a model of progressive renal interstitial fibrosis, results in rapid parenchymal deterioration. Atubular glomeruli are formed in many renal disorders, but their identification has been limited by labor-intensive available techniques. The formation of atubular glomeruli was therefore investigated in adult male mice subjected to complete UUO under general anesthesia. In this species, the urinary pole of Bowman's capsule is normally lined by tall parietal epithelial cells similar to those of the proximal tubule, and both avidly bind Lotus tetragonolobus lectin. Following UUO, these cells became flattened, lost their affinity for Lotus lectin, and no longer generated superoxide (revealed by nitroblue tetrazolium infusion). Based on Lotus lectin staining, stereological measurements, and serial section analysis, over 80% of glomeruli underwent marked transformation after 14 days of UUO. The glomerulotubular junction became stenotic and atrophic due to cell death by apoptosis and autophagy, with concomitant remodeling of Bowman's capsule to form atubular glomeruli. In this degenerative process, transformed epithelial cells sealing the urinary pole expressed α-smooth muscle actin, vimentin, and nestin. Although atubular glomeruli remained perfused, renin immunostaining was markedly increased along afferent arterioles, and associated maculae densae disappeared. Numerous progressive kidney disorders, including diabetic nephropathy, are characterized by the formation of atubular glomeruli. The rapidity with which glomerulotubular junctions degenerate, coupled with Lotus lectin as a marker of glomerular integrity, points to new investigative uses for the model of murine UUO focusing on mechanisms of epithelial cell injury and remodeling in addition to fibrogenesis.

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49

Rofananda, Ihsan Fahmi, Jusak Nugraha, Imam Susilo, and Miyayu Soneta Sofyan. "Effect of Glutamine on Apoptosis-inducing Factor Expression and Apoptosis of Glomerular Parietal Epithelial Cells of Cisplatin-exposed Rats." Open Access Macedonian Journal of Medical Sciences 9, A (May 14, 2021): 367–72. http://dx.doi.org/10.3889/oamjms.2021.5915.

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AIM: This study analyzed the nephroprotective effect by examining apoptosis-inducing factor (AIF) expression and apoptosis rate in the glomerular parietal epithelial cell of cisplatin-exposed rats. METHODS: Samples consisted of 30 rats (divided into 3 groups: Group P0 received no treatment, group P1 received a cisplatin injection on the 7th day, and group P2 received glutamine injection on days 1–7 and cisplatin injection on the 7th day). After 72 h, the tissue samples were immunohistochemically processed. AIF expression was measured in an Allred score. The apoptosis rate was measured in apoptotic cells/field of view. Statistical analysis was carried out using JASP Statistics ver. 0.12.0 (p < 0.05). RESULTS: AIF expression values are follows: P0 = 4.89 ± 0.418, P1 = 6.14 ± 0.685, and P2 = 4.95 ± 0.530. The Kruskal–Wallis test result showed a significant difference (p < 0.05) between the groups and Dunn’s post hoc test showed a significant difference between P0 and P1 and between P1 and P2, but no significant difference between P0 and P2. Meanwhile, apoptosis rate values are as follows: P0 = 24.3 ± 9.821, P1 = 123.6 ± 16.008, and P2 = 77.2 ± 10.644. The Kruskal–Wallis test result showed a significant difference (p < 0.05) between the groups, and Dunn’s post hoc test showed a significant difference between P0 and P1, between P1 and P2, and between P0 and P2. CONCLUSION: The expression of AIF and apoptosis of glomerular parietal epithelial cells of the cisplatin-exposed rat has decreased after glutamine treatment.

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Yadav, Anju, Sridevi Vallabu, Dileep Kumar, Guohua Ding, Douglas N. Charney, Praveen N. Chander, and Pravin C. Singhal. "HIVAN phenotype: consequence of epithelial mesenchymal transdifferentiation." American Journal of Physiology-Renal Physiology 298, no. 3 (March 2010): F734—F744. http://dx.doi.org/10.1152/ajprenal.00415.2009.

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Анотація:

Human immunodeficiency virus (HIV)-1-associated nephropathy (HIVAN) is characterized by proliferation of glomerular and tubular epithelial cells. We studied the role of epithelial mesenchymal transdifferentiation (EMT) in the development of HIVAN phenotype. Renal cortical sections from six FVB/N (control) and six Tg26 (HIVAN) mice were immunolabeled for PCNA, α-smooth muscle actin (α-SMA), fibroblast-specific protein-1 (FSP1), CD3, and F4/80. Since periglomerular cells (PGCs) and peritubular cells (PTCs) did not show any labeling for CD3 and F4/80 but showed labeling for α-SMA or FSP1, it appears that these were myofibroblasts that migrated from either glomerular or tubular sites, respectively. Occurrence of EMT was also supported by diminished expression of E-cadherin by renal epithelial cells in Tg26 mice. Interestingly, Tg26 mice also showed enhanced renal tissue expression of ZEB2; henceforth, it appears that transcription of molecules required for maintenance of de novo renal epithelial cell phenotype was suppressed. To evaluate the role of ANG II, Tg26 mice in groups of three were administered either normal saline or telmisartan (an AT1 receptor blocker) for 2 wk, followed by evaluation for renal cell EMT. Renal cortical section of Tg26 mice showed a sevenfold increase ( P < 0.001) in parietal epithelial cell (PEC)-PGC and a threefold increase ( P < 0.01) in tubular cell (TC)-PTC proliferation (PCNA-positive cells). Similarly, both PECs-PGCs and TCs-PTCs in Tg26 mice showed enhanced expression of α-SMA and FSP1. Both PECs and podocytes contributed to the glomerular proliferative phenotype, but the contribution of PECs was much greater. Telmisartan-receiving Tg26 mice (TRM) showed attenuated number of proliferating PECs-PGCs and TCs-PTCs compared with saline-receiving Tg26 mice (SRM). Similarly, TRM showed diminished expression of α-SMA and FSP1 by both PECs-PGCs and TCs-PTCs compared with SRM. We conclude that EMT contributes to the manifestation of the proliferative phenotype in HIVAN mice.

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