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  • 1
    Online Resource
    Online Resource
    Urinary proteomic analysis of chronic allograft nephropathy
    Wiley ; 2008
    In:  PROTEOMICS – Clinical Applications Vol. 2, No. 7-8 ( 2008-07), p. 1025-1035
    Details
    In: PROTEOMICS – Clinical Applications, Wiley, Vol. 2, No. 7-8 ( 2008-07), p. 1025-1035
    Abstract: The pathogenesis of progressive renal allograft injury, which is termed chronic allograft nephropathy (CAN), remains obscure and is currently defined by histology. Prospective protocol‐biopsy trials have demonstrated that clinical and standard laboratory tests are insufficiently sensitive indicators of the development and progression of CAN. The study aim was to determine if CAN could be characterized by urinary proteomic data and identify the proteins associated with disease. The urinary proteome of 75 renal transplant recipients and 20 healthy volunteers was analyzed using surface enhanced laser desorption and ionization MS. Patients could be classified into subgroups with normal histology and Banff CAN grades 2‐3 with a sensitivity of 86% and a specificity of 92% by applying the classification algorithm Adaboost to urinary proteomic data. Several urinary proteins associated with advanced CAN were identified including α1‐microglobulin, β2‐microglobulin, prealbumin, and endorepellin, the antiangiogenic C‐terminal fragment of perlecan. Increased urinary endorepellin was confirmed by ELISA and increased tissue expression of the endorepellin/perlecan ratio by immunofluoresence analysis of renal biopsies. In conclusion, analysis of urinary proteomic data has further characterized the more severe CAN grades and identified urinary endorepellin, as a potential biomarker of advanced CAN.
    Type of Medium: Online Resource
    ISSN: 1862-8346 , 1862-8354
    URL: Issue
    URL: Article
    DOI: 10.1002/prca.v2:7/8
    DOI: 10.1002/prca.200780137
    Language: English
    Publisher: Wiley
    Publication Date: 2008
    detail.hit.zdb_id: 2317130-3
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  • 2
    Online Resource
    Online Resource
    Aldosterone induces mesangial cell apoptosis both in vivo and in vitro
    American Physiological Society ; 2008
    In:  American Journal of Physiology-Renal Physiology Vol. 295, No. 1 ( 2008-07), p. F73-F81
    Details
    In: American Journal of Physiology-Renal Physiology, American Physiological Society, Vol. 295, No. 1 ( 2008-07), p. F73-F81
    Abstract: Both clinical and experimental reports indicate that aldosterone contributes to the progression of renal failure independent of its hemodynamic effects. In the present study, we evaluated effect of aldosterone on human mesangial cell (MC) growth. Aldosterone induced apoptotic and mitogenic effects on MCs. Aldosterone promoted MC apoptosis in a dose- and time-dependent manner. Spironolactone, a mineralocorticoid receptor antagonist, inhibited aldosterone-induced MC apoptosis. Similarly, antioxidants and free radical scavengers partially attenuated proapoaptotic effects of aldosterone. Aldosterone also enhanced dephosphorylation of phospho-Bad and accumulation of cytosolic cytochrome c in MCs. In in vivo studies, rats were randomly assigned to receive normal saline, aldosterone, or eplerenone + aldosterone for 28 days. Systolic blood pressure, urinary albumin excretion rate, serum creatinine, and aldosterone were measured. Aldosterone-infused rats developed elevated systolic blood pressure and albuminuria when compared with control rats. Aldosterone-treated rats also showed greater numbers of apoptosed MCs. This proapoptotic effect of aldosterone was inhibited by eplerenone, a selective aldosterone antagonist. These findings suggest that aldosterone, besides its hemodynamic effects, may also directly contribute to the occurrence of MC apoptosis.
    Type of Medium: Online Resource
    ISSN: 1931-857X , 1522-1466
    URL: Article
    DOI: 10.1152/ajprenal.00435.2007
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2008
    detail.hit.zdb_id: 1477287-5
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  • 3
    Online Resource
    Online Resource
    HIVAN phenotype: consequence of epithelial mesenchymal transdifferentiation
    American Physiological Society ; 2010
    In:  American Journal of Physiology-Renal Physiology Vol. 298, No. 3 ( 2010-03), p. F734-F744
    Details
    In: American Journal of Physiology-Renal Physiology, American Physiological Society, Vol. 298, No. 3 ( 2010-03), p. F734-F744
    Abstract: 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 AT 1 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.
    Type of Medium: Online Resource
    ISSN: 1931-857X , 1522-1466
    URL: Article
    DOI: 10.1152/ajprenal.00415.2009
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2010
    detail.hit.zdb_id: 1477287-5
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  • 4
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    Online Resource
    Nephropathy in Zucker Diabetic Fat Rat Is Associated with Oxidative and Nitrosative Stress : Prevention by Chronic Therapy with a Peroxynitrite Scavenger Ebselen
    Ovid Technologies (Wolters Kluwer Health) ; 2004
    In:  Journal of the American Society of Nephrology Vol. 15, No. 9 ( 2004-09), p. 2391-2403
    Details
    In: Journal of the American Society of Nephrology, Ovid Technologies (Wolters Kluwer Health), Vol. 15, No. 9 ( 2004-09), p. 2391-2403
    Type of Medium: Online Resource
    ISSN: 1046-6673
    URL: Article
    DOI: 10.1097/01.ASN.0000135971.88164.2C
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2004
    detail.hit.zdb_id: 2029124-3
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  • 5
    Online Resource
    Online Resource
    Estrogen promotes microvascular pathology in female stroke-prone spontaneously hypertensive rats
    American Physiological Society ; 2003
    In:  American Journal of Physiology-Endocrinology and Metabolism Vol. 285, No. 1 ( 2003-07), p. E232-E239
    Details
    In: American Journal of Physiology-Endocrinology and Metabolism, American Physiological Society, Vol. 285, No. 1 ( 2003-07), p. E232-E239
    Abstract: Estrogen produces both beneficial and adverse effects on cardiovascular health via mechanisms that remain unclear. Stroke-prone spontaneously hypertensive rats (SHRSP) maintained on Stroke-Prone Rodent Diet and 1% NaCl drinking water (starting at 8 wk of age) rapidly develop stroke and malignant nephrosclerosis that can be prevented, despite continued hypertension, by drugs targeting angiotensin II and aldosterone actions. This study evaluated estrogen's effects in the SHRSP model. Female SHRSP that were sham operated (SHAM), ovariectomized (OVX) at 4 wk of age, or OVX and treated with estradiol benzoate (E 2 ,30 μg·kg -1 ·wk -1 ) were studied. In a survival protocol, OVX rats lived significantly longer (15.1 ± 0.3 wk) compared with SHAM (13.6 ± 0.2 wk) or OVX+E 2 rats (12.4 ± 0.2 wk). In a protocol in which animals were matched for age, at 11.5 wk, terminal systolic blood pressure and urine protein excretion were elevated in SHAM and OVX+E 2 rats compared with OVX rats; blood urea nitrogen, renal microvascular and glomerular lesions, and plasma renin concentration were elevated in OVX+E 2 relative to SHAM or OVX rats. In a survival protocol using intact female SHRSP, treatment with an antiestrogen (tamoxifen, 7 mg·kg -1 ·wk -1 ) prolonged survival by 〉 2 wk compared with controls ( P 〈 0.01). The data indicate that estrogen promotes microangiopathy in the kidney and stroke in saline-drinking SHRSP.
    Type of Medium: Online Resource
    ISSN: 0193-1849 , 1522-1555
    URL: Article
    DOI: 10.1152/ajpendo.00029.2003
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2003
    detail.hit.zdb_id: 1477331-4
    SSG: 12
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  • 6
    Online Resource
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    Aldosterone, but not angiotensin II, increases profibrotic factors in kidney of adrenalectomized stroke-prone spontaneously hypertensive rats
    American Physiological Society ; 2008
    In:  American Journal of Physiology-Endocrinology and Metabolism Vol. 295, No. 2 ( 2008-08), p. E305-E312
    Details
    In: American Journal of Physiology-Endocrinology and Metabolism, American Physiological Society, Vol. 295, No. 2 ( 2008-08), p. E305-E312
    Abstract: An increase in angiotensin II (ANG II) under conditions of high salt intake can result in renal damage. The extent to which ANG II does this directly or by way of stimulating aldosterone (Aldo) secretion is a subject of some debate. In the present study, we sought to determine the separate effects of Aldo and ANG II on the expression of plasminogen activator inhibitor-1 (PAI-1) and other factors related to renal fibrosis in the stroke-prone spontaneously hypertensive rat (SHRSP). Saline-drinking male SHRSPs underwent adrenalectomy (ADX) or sham operation (Sham). Treatment groups consisted of ADX + ANG II (25 ng/min sc) and ADX + Aldo (40 μg·kg −1 ·day −1 sc). After 2 wk of treatment, circulating Aldo levels were reduced to the limit of detection, renal PAI-1, transforming growth factor-β1 (TGF-β1), and osteopontin expression, and phospho-Smad2 (p-Smad2) level were decreased severalfold, and Smad7 (an inhibitory regulator of TGF-β1 action) expression was increased in ADX compared with Sham rats. Infusion of Aldo into ADX SHRSPs restored the renal mRNA expression of PAI-1, TGF-β1 (along with restored p-Smad2 level), and osteopontin and reduced that of Smad7, whereas ANG II had no or a lesser effect. The findings were confirmed by histological examination of renal tissue. In summary, in the saline-drinking SHRSP, Aldo increased renal profibrotic factors and produced renal injury whereas ANG II in the absence of the adrenals had no effect.
    Type of Medium: Online Resource
    ISSN: 0193-1849 , 1522-1555
    URL: Article
    DOI: 10.1152/ajpendo.00512.2007
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2008
    detail.hit.zdb_id: 1477331-4
    SSG: 12
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  • 7
    Online Resource
    Online Resource
    Human immunodeficiency virus downregulates podocyte apoE expression
    American Physiological Society ; 2009
    In:  American Journal of Physiology-Renal Physiology Vol. 297, No. 3 ( 2009-09), p. F653-F661
    Details
    In: American Journal of Physiology-Renal Physiology, American Physiological Society, Vol. 297, No. 3 ( 2009-09), p. F653-F661
    Abstract: Apolipoprotein E ( apoE) has been demonstrated to play an important role in providing protection against mesangial cell injury. In the present study, we evaluated the role of apoE and its associated downstream effects in human immunodeficiency virus (HIV)-associated nephropathy (HIVAN). Control ( n = 6) and age- and sex-matched HIV-1 transgenic mice (Tg26, n = 6) were evaluated for their renal cortical expression of apoE. Renal tissue from Tg26 mice not only showed decreased apoE expression but also displayed downregulation of perlecan mRNA expression. In in vitro studies, conditionally immortalized human podocytes (CIHPs) were transduced with either NL4-3HIV (an HIV-1 construct lacking gag and pol, used for the development of Tg26 mouse model; NL4-3/CIHP) or empty vector (EV/CIHP); NL4-3/CIHPs and EV/CIHPs were studied for apoE mRNA expression. NL4-3/CIHPs showed reduction in apoE expression compared with EV/CIHPs. To evaluate the role of HIV-1 genes in the modulation of apoE expression, conditionally immortalized mouse podocytes (CIMPs) were transduced with individual HIV-1 gene constructs. Only nef-transduced CIMPs showed a decrease in apoE expression. To confirm this effect of nef in CIHPs, microarray analysis was performed in stable colonies of nef/CIHPs and EV/CIHPs. nef/CIHPs showed a 60% decrease in apoE and a 90% reduction in heparan sulfate mRNA expression. Moreover, nef transgenic mice showed a decrease in renal tissue expression of both apoE and perlecan. Both Tg26 and nef transgenic mice also showed areas of mesangial cell proliferation. These findings suggest that HIV-1-induced reduction in podocyte apoE expression and associated downregulation of podocyte perlecan might be contributing to mesangial cell (MC) phenotype in HIVAN.
    Type of Medium: Online Resource
    ISSN: 1931-857X , 1522-1466
    URL: Article
    DOI: 10.1152/ajprenal.90668.2008
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2009
    detail.hit.zdb_id: 1477287-5
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  • 8
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    Online Resource
    Pharmacological manipulation of arachidonic acid-epoxygenase results in divergent effects on renal damage
    Frontiers Media SA ; 2014
    In:  Frontiers in Pharmacology Vol. 5 ( 2014-08-15)
    Details
    In: Frontiers in Pharmacology, Frontiers Media SA, Vol. 5 ( 2014-08-15)
    Type of Medium: Online Resource
    ISSN: 1663-9812
    URL: Article
    DOI: 10.3389/fphar.2014.00187
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2014
    detail.hit.zdb_id: 2587355-6
    SSG: 15,3
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  • 9
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    Online Resource
    Parietal Epithelial Cell Behavior and Its Modulation by microRNA-193a
    MDPI AG ; 2023
    In:  Biomolecules Vol. 13, No. 2 ( 2023-01-31), p. 266-
    Details
    In: Biomolecules, MDPI AG, Vol. 13, No. 2 ( 2023-01-31), p. 266-
    Abstract: 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.
    Type of Medium: Online Resource
    ISSN: 2218-273X
    URL: Article
    DOI: 10.3390/biom13020266
    Language: English
    Publisher: MDPI AG
    Publication Date: 2023
    detail.hit.zdb_id: 2701262-1
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  • 10
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    Online Resource
    Disruption of APOL1-miR193a Axis Induces Disorganization of Podocyte Actin Cytoskeleton
    Springer Science and Business Media LLC ; 2019
    In:  Scientific Reports Vol. 9, No. 1 ( 2019-03-05)
    Details
    In: Scientific Reports, Springer Science and Business Media LLC, Vol. 9, No. 1 ( 2019-03-05)
    Abstract: APOL1-miR193a axis participates in the preservation of molecular phenotype of differentiated podocytes (DPDs). We examined the hypothesis that APOL1 (G0) preserves, but APOL1 risk alleles (G1 and G2) disrupt APOL1-miR193a axis in DPDs. DPDG0s displayed down-regulation of miR193a, but upregulation of nephrin expression. DPDG1s/G2s exhibited an increase in miR193a and down-regulation of the expression of adherens complex’s constituents (CD2AP, nephrin, and dendrin). DPDG0s showed decreased Cathepsin L, enhanced dynamin expressions, and the intact actin cytoskeleton. On the contrary, DPDG1s/G2s displayed an increase in Cathepsin L, but down-regulation of dynamin expressions and disorganization of the actin cytoskeleton. APOL1 silencing enhanced miR193a and Cathepsin L, but down-regulated dynamin expressions. DPDG1s/G2s displayed nuclear import of dendrin, indicating an occurrence of destabilization of adherens complexes in APOL1 risk milieu. These findings suggest that DPDG1s and DPDG2s developed disorganized actin cytoskeleton as a consequence of disrupted APOL1-miR193a axis. Interestingly, docking and co-labeling studies suggested an interaction between APOL1 and CD2AP. APOL1 G1 / G1 and APOL1 G1 / G2 transgenic mice displayed nuclear import of dendrin indicating destabilization of adherens complexes in podocytes; moreover, these mice showed a four-fold increase in urinary albumin to creatinine ratio and development of focal segmental glomerular lesions.
    Type of Medium: Online Resource
    ISSN: 2045-2322
    URL: Article
    DOI: 10.1038/s41598-019-39376-y
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2019
    detail.hit.zdb_id: 2615211-3
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