scholarly journals Apolipoprotein L1 Dynamics in Human Parietal Epithelial Cell Molecular Phenotype Kinetics

2018 ◽  
Author(s):  
Vinod Kumar ◽  
Himanshu Vashistha ◽  
Xiqian Lan ◽  
Nirupama Chandel ◽  
Kamesh Ayasolla ◽  
...  
Keyword(s):  
Vitamin D ◽  
Epithelial Cell ◽  
Transgenic Mice ◽  
Vitamin D Receptor ◽  
Receptor Agonist ◽  
Feedback Loop ◽  
Molecular Phenotype ◽  
Parietal Epithelial Cell ◽  
Parietal Epithelial Cells ◽  
Apolipoprotein L1

AbstractHuman Parietal Epithelial cells (PECs) are considered as a source of progenitor cells to sustain podocyte (PD) homeostasis. We hypothesized that the absence of apolipoprotein (APO) L1 favors the PEC phenotype and that induction of APOL1 transitions to PD renewal. During PECs’ transition, APOL1 expression coincided with the expression of PD markers (PEC transition) along with down regulation of miR193a. The induction of APOL1 down regulated miR193a and induced PD markers in PECs/HEKs; whereas, the APOL1-silencing in transited (Tr)-PECs/HepG2s up regulated miR193a expression suggesting a reciprocally linked feedback loop relationship between APOL1 and miR193a. HIV, IFN-y, and vitamin D receptor agonist (VDA) induced APOL1 expression and PEC transition markers but down regulated miR193a in PECs/HEKs. Glomeruli in HIV patients and HIV: APOL1 transgenic mice displayed foci of PECs expressing synaptopodin, a PEC transition marker. Since APOL1 silencing in PECs partially attenuated HIV-, VDA-, and IFN-y-induced PECs transition, this would suggest that APOL1 is an important functional constituent of APOL1-miR193a axis.

scholarly journals The selective vitamin D receptor agonist, elocalcitol, reduces endometriosis development in a mouse model by inhibiting peritoneal inflammation

2012 ◽  
Vol 27 (7) ◽  
pp. 2010-2019 ◽  
Author(s):  
M. Mariani ◽  
P. Vigano ◽  
D. Gentilini ◽  
B. Camisa ◽  
E. Caporizzo ◽  
...  
Keyword(s):  
Vitamin D ◽  
Mouse Model ◽  
Vitamin D Receptor ◽  
Receptor Agonist ◽  
Peritoneal Inflammation

scholarly journals New Insights into Glomerular Parietal Epithelial Cell Activation and Its Signaling Pathways in Glomerular Diseases

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Hua Su ◽  
Shan Chen ◽  
Fang-Fang He ◽  
Yu-Mei Wang ◽  
Philip Bondzie ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Signaling Pathways ◽  
Membranous Nephropathy ◽  
Cell Activation ◽  
Crescentic Glomerulonephritis ◽  
Diabetic Glomerulopathy ◽  
Glomerular Diseases ◽  
The Past ◽  
Parietal Epithelial Cell ◽  
Parietal Epithelial Cells

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.

scholarly journals Cells of NG2 lineage increase in glomeruli of mice following podocyte depletion

2018 ◽  
Vol 315 (5) ◽  
pp. F1449-F1464 ◽  
Author(s):  
Taihei Suzuki ◽  
Diana G. Eng ◽  
Aaron D. McClelland ◽  
Jeffrey W. Pippin ◽  
Stuart J. Shankland
Keyword(s):  
Epithelial Cell ◽  
Cell Types ◽  
Lineage Tracing ◽  
Cell Fates ◽  
Kinase Substrate ◽  
Parietal Epithelial Cell ◽  
Fluorescence Protein ◽  
Red Fluorescence Protein ◽  
Podocyte Proteins ◽  
Parietal Epithelial Cells

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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