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MicroRNA Expression Profiles of Human iPS Cells, Retinal Pigment Epithelium Derived From iPS, and Fetal Retinal Pigment Epithelium
Published on: June 24, 2014
Parietal Epithelial Cell Behavior and Its Modulation by microRNA-193a.
Joyita Bharati1,2, Praveen N Chander3, Pravin C Singhal1
1Institute of Molecular Medicine, Feinstein Institute for Medical Research and Department of Medicine, Zucker School of Medicine at Hofstra-Northwell, Hempstead, NY 11549, USA.
Glomerular parietal epithelial cells (PECs) play dual roles in kidney health and disease. MicroRNA-193a (miR193a) influences PEC behavior, impacting conditions like focal segmental glomerulosclerosis and crescentic glomerulonephritis.
Area of Science:
- Nephrology
- Cell Biology
- Molecular Medicine
Background:
- Glomerular parietal epithelial cells (PECs) exhibit both reparative and pathogenic functions.
- Activated PECs contribute to glomerular diseases such as focal segmental glomerulosclerosis (FSGS) and crescentic glomerulonephritis (CrescGN).
- The behavior of PECs is modulated by the local microenvironment and specific mediators.
Purpose of the Study:
- To review the critical roles of PECs in glomerular health and disease.
- To explore the influence of microRNA-193a (miR193a) on PEC behavior and kidney pathology.
- To highlight the dual nature of PECs as potentially reparative or pathogenic.
Main Methods:
- Literature review of recent studies on PECs and miR193a.
- Analysis of findings from animal models of FSGS and CrescGN.
- Inclusion of in vitro evidence regarding PEC trans-differentiation.
Main Results:
- PECs can adopt a podocyte phenotype during glomerular development and injury, suggesting a reparative capacity.
- Aberrant PEC activation contributes to extracapillary proliferation in FSGS and CrescGN.
- miR193a is implicated in FSGS pathogenesis by downregulating Wilms' tumor protein and causing podocyte dedifferentiation.
- Inhibition of miR193a ameliorates crescent formation in CrescGN models.
- Downregulation of miR193a promotes PEC trans-differentiation into podocytes in vitro.
Conclusions:
- PECs possess a dynamic behavior that can be either beneficial or detrimental to kidney function.
- miR193a acts as a key regulator of PEC phenotype and function.
- Targeting miR193a may offer therapeutic strategies for glomerular diseases characterized by PEC dysfunction.
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