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 Parietal epithelial cell dysfunction in crescentic glomerulonephritis

2021 ◽  
Author(s):  
Milagros N. Wong ◽  
Pierre-Louis Tharaux ◽  
Florian Grahammer ◽  
Victor G. Puelles
Keyword(s):  
Epithelial Cell ◽  
Cell Biology ◽  
Immune Modulation ◽  
Crescentic Glomerulonephritis ◽  
Kidney Diseases ◽  
Crescent Formation ◽  
Glomerular Lesion ◽  
Cell Dysfunction ◽  
Parietal Epithelial Cell ◽  
Parietal Epithelial Cells

AbstractCrescentic glomerulonephritis represents a group of kidney diseases characterized by rapid loss of kidney function and the formation of glomerular crescents. While the role of the immune system has been extensively studied in relation to the development of crescents, recent findings show that parietal epithelial cells play a key role in the pathophysiology of crescent formation, even in the absence of immune modulation. This review highlights our current understanding of parietal epithelial cell biology and the reported physiological and pathological roles that these cells play in glomerular lesion formation, especially in the context of crescentic glomerulonephritis.

Glomerular Outgrowth as an Ex Vivo Assay to Analyze Pathways Involved in Parietal Epithelial Cell Activation

10.3791/60324 ◽  
2020 ◽  
Author(s):  
Jennifer Eymael ◽  
Laura Miesen ◽  
Fieke Mooren ◽  
Jitske Jansen ◽  
Jack Wetzels ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Cell Activation ◽  
Ex Vivo ◽  
Parietal Epithelial Cell ◽  
Ex Vivo Assay

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.

The Primary Glomerular Diseases

2017 ◽  
Author(s):  
Richard J. Glassock ◽  
Sanjeev Sethi ◽  
Fernando C. Fervenza
Keyword(s):  
Renal Biopsy ◽  
Membranous Nephropathy ◽  
Minimal Change Disease ◽  
Crescentic Glomerulonephritis ◽  
Minimal Change ◽  
C3 Glomerulonephritis ◽  
Focal And Segmental Glomerulosclerosis ◽  
Glomerular Diseases ◽  
Dense Deposit ◽  
Primary Glomerular Diseases

Glomerular disorders in which the manifestations of disease are primarily confined to the kidneys, without multisystem involvement, are not only common but very heterogeneous in terms of pathogenesis and clinical features. Typically, these primary glomerular diseases are characterized according to the findings on renal biopsy, as studied by light, immunofluorescence, and electron microscopy. The principal primary glomerular diseases are minimal change disease, focal and segmental glomerulosclerosis, membranous nephropathy, C3 glomerulonephritis and dense deposit disease, IgA nephropathy, and renal-limited crescentic glomerulonephritis. These clinicopathologic entities are discussed according to epidemiology, clinical features, pathology, pathogenesis (and genetics if appropriate), prognosis, and treatment, emphasizing recent findings.  Key words: C3 glomerulonephritis, dense deposit disease, focal and segmental glomerulosclerosis, glomerulonephritis, IgA nephropathy, membranous nephropathy, minimal change disease, renal biopsy, renal-limited crescentic glomerulonephritis

scholarly journals For better or worse: a niche for Notch in parietal epithelial cell activation

2013 ◽  
Vol 83 (6) ◽  
pp. 988-990 ◽  
Author(s):  
Mariya T. Sweetwyne ◽  
Katalin Susztak
Keyword(s):  
Epithelial Cell ◽  
Cell Activation ◽  
Parietal Epithelial Cell

scholarly journals Nature and Mediators of Parietal Epithelial Cell Activation in Glomerulonephritides of Human and Rat

2013 ◽  
Vol 183 (6) ◽  
pp. 1769-1778 ◽  
Author(s):  
Paola Rizzo ◽  
Norberto Perico ◽  
Elena Gagliardini ◽  
Rubina Novelli ◽  
Malcolm R. Alison ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Cell Activation ◽  
Parietal Epithelial Cell

scholarly journals Parietal Epithelial Cell Activation Marker in Early Recurrence of FSGS in the Transplant

2012 ◽  
Vol 7 (11) ◽  
pp. 1852-1858 ◽  
Author(s):  
Huma Fatima ◽  
Marcus J. Moeller ◽  
Bart Smeets ◽  
Hai-Chun Yang ◽  
Vivette D. D’Agati ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Cell Activation ◽  
Early Recurrence ◽  
Activation Marker ◽  
Cell Activation Marker ◽  
Parietal Epithelial Cell

scholarly journals Endothelial Epas1 Deficiency Is Sufficient To Promote Parietal Epithelial Cell Activation and FSGS in Experimental Hypertension

2017 ◽  
Vol 28 (12) ◽  
pp. 3563-3578 ◽  
Author(s):  
Yosu Luque ◽  
Olivia Lenoir ◽  
Philippe Bonnin ◽  
Lise Hardy ◽  
Anna Chipont ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Cell Activation ◽  
Experimental Hypertension ◽  
Parietal Epithelial Cell
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