scholarly journals CD44 impacts glomerular parietal epithelial cell changes in the aged mouse kidney

2020 ◽  
Vol 8 (12) ◽  
Author(s):  
Hiroko Hamatani ◽  
Diana G. Eng ◽  
Keiju Hiromura ◽  
Jeffrey W. Pippin ◽  
Stuart J. Shankland

Aging ◽  
2020 ◽  
Vol 12 (17) ◽  
pp. 17601-17624 ◽  
Author(s):  
Natalya V. Kaverina ◽  
Diana G. Eng ◽  
Jeffrey H. Miner ◽  
Jeffrey W. Pippin ◽  
Stuart J. Shankland


Author(s):  
Jennifer Eymael ◽  
Laura Miesen ◽  
Fieke Mooren ◽  
Jitske Jansen ◽  
Jack Wetzels ◽  
...  


2020 ◽  
Vol 75 (5) ◽  
pp. 812-814
Author(s):  
Bart Smeets ◽  
Laura Miesen ◽  
Stuart J. Shankland


2019 ◽  
Vol 317 (6) ◽  
pp. F1680-F1694 ◽  
Author(s):  
Gek Cher Chan ◽  
Diana G. Eng ◽  
Jeffrey H. Miner ◽  
Charles E. Alpers ◽  
Kelly Hudkins ◽  
...  

In healthy glomeruli, parietal epithelial cell (PEC)-derived extracellular matrix (ECM) proteins include laminin-β1, perlecan, and collagen type IV-α2 and podocyte-specific ECM proteins include laminin-β2, agrin, and collagen type IV-α4. This study aimed to define individual ECM protein isoform expression by PECs in both experimental and human focal segmental glomerulosclerosis (FSGS) and diabetic nephropathy (DN) and to determine if changes were CD44 dependent. In experimental FSGS induced with a cytotoxic podocyte antibody and in the BTBR ob/ob mouse model of DN, PEC-derived protein staining was significantly increased in PECs. Dual staining also showed de novo expression of the podocyte-specific ECM proteins laminin-β2 and agrin in PECs. Similar findings were observed in biopsies from patients with FSGS and DN. Increases in individual ECM proteins colocalized with CD44 in PECs in disease. To determine the role of CD44, FSGS was induced in CD44−/− and CD44+/+ mice. PEC staining for perlecan, collagen type IV-α2, laminin-β2, and agrin were significantly lower in diseased CD44−/− mice compared with diseased CD44+/+ mice. These results show that in experimental and human FSGS and DN, PECs typically in an activated state, produce both PEC-derived and podocyte-specific ECM protein isoforms, and that the majority of these changes were dependent on CD44.



2014 ◽  
Vol 307 (7) ◽  
pp. F798-F799 ◽  
Author(s):  
Bart Smeets ◽  
Tobias B. Huber


2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Hua Su ◽  
Shan Chen ◽  
Fang-Fang He ◽  
Yu-Mei Wang ◽  
Philip Bondzie ◽  
...  

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.



2018 ◽  
Vol 315 (5) ◽  
pp. F1449-F1464 ◽  
Author(s):  
Taihei Suzuki ◽  
Diana G. Eng ◽  
Aaron D. McClelland ◽  
Jeffrey W. Pippin ◽  
Stuart J. Shankland

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.



1909 ◽  
Vol 6 (1) ◽  
pp. 1-16 ◽  
Author(s):  
J. Ewing
Keyword(s):  


2014 ◽  
Vol 247 (8) ◽  
pp. 675-683 ◽  
Author(s):  
Niloofar M. Tabatabai ◽  
Paula E. North ◽  
Kevin R. Regner ◽  
Suresh N. Kumar ◽  
Christine B. Duris ◽  
...  


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