Abstract
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.
Highlights
The glomerulus comprises four types of intrinsic cells including endothelial cells, mesangial cells, podocytes, and parietal epithelial cells (PECs)
There are numerous studies focused on the biological functions and pathogenic roles of the first three cells, whereas PEC, which lines along Bowman’s capsule, until recently has aroused scientific interest leading to the exploration of its physiological and pathological effects especially in several forms of glomerular diseases, such as crescentic glomerulonephritis (CGN), focal segmental glomerulosclerosis (FSGS), and diabetic nephropathy (DN)
This study strongly suggests that,in Collapsing variant of focal segmental glomerulosclerosis (cFSGS), proliferating epithelial cells originate from PECs rather than from hyperplastic podocytes de novo expressing the PECs phenotype
Summary
The glomerulus comprises four types of intrinsic cells including endothelial cells, mesangial cells, podocytes, and parietal epithelial cells (PECs). Cellular crescent is the typical morphological change observed in CGN It is defined as the multilayered accumulations of PECs and other cell types within Bowman’s space. The authors proposed that glomerular PECs could function as a progenitor cell niche for podocytes and under proper settings could proliferate and transdifferentiate into podocytes, which may be a pivotal factor for the regression of DN [31] In another DN animal model, activated and proliferating PECs were observed and associated with overexpressed kidney injury molecule 1 which positively correlated with the extent of proteinuria and podocytopenia in diabetes [32]. The endothelium is severely injured in the late phase of diabetic status, which leads to leakage of plasma and induces PEC activation and pseudocrescent formation, partially resembling the mechanisms which account for cellular crescents development in inflammatory CGN. The mechanisms are not known currently; the activation of PEC may be triggered by the injury of podocyte or endothelium and the seepage of plasma
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