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Abstract: SA-PO359

HIV-Induced Parietal Epithelial Cell Proliferation: Role of miR193a

Session Information

Category: Glomerular Diseases

  • 1202 Glomerular Diseases: Immunology and Inflammation


  • Kumar, Vinod, Fienstine Institute for Medical Research, NEW YORK, New York, United States
  • Paliwal, Nitpriya, Feinstein Institute for Medical Research, Manhasset, New York, United States
  • Lan, Xiqian, Feinstein Institute for Medical Research, Manhasset, New York, United States
  • Ayasolla, Kamesh R., Feinstein Institute for Medical Research, Manhasset, New York, United States
  • Chowdhary, Sheetal, Feinstein Institute of Medical Research, New Hyde Park, New York, United States
  • Marashi Shoshtari, Seyedeh Shadafarin, The Feinstein Institute for Medical Research, Manhasset, New York, United States
  • Malhotra, Ashwani, Feinstein Institute Medical Research and NSLIJ, MANHASSET, New York, United States
  • Meyer-Schwesinger, Catherine, University of Hamburg, Hamburg, Germany
  • Skorecki, Karl, Rambam Health Care Campus, Haifa, Israel
  • Singhal, Pravin C., North Shore LIJ Health System, Great Neck, New York, United States

miR193a has been reported to play an important role in the determination of glomerular epithelial cells' phenotype. miR193a is a tumor suppressor gene and its downregulation has been associated with enhanced cellular proliferation. HIV-associated nephropathy (HIVAN) is characterized by an accumulation of proliferating parietal epithelial cells (PECs) in the Bowman's space; however, the involved mechanism is not clear. Since HIV down-regulates the expression of miR193a, we asked whether HIV is stimulating PECs proliferation through down-regulation of miR193a.


Immortalized PECs were transduced with vector (PECV) or different concentrations of HIV (104, 103, 102, and 101 GEU/ml; PECHIV) followed by growth arrest (24 hours), followed by incubation in media containing 1% serum for 48 hours (n=4). Cell growth was assayed by cell count and MTT assay. To determine the role of miR193a, PECVs and PECHIV were transduced with empty vector (25 nM), miR193a (25 nM), an inhibitor of miR193a (25 nM) plasmids (n=4). After 48 hours, proteins and RNAs were extracted. Protein blots were probed for molecular markers of mTOR (p-mTOR, p-70S6K, p-4EBP, and p-eEF) and epithelial-mesenchymal transition (α-SMA, SNAIL, and fibronectin; EMT) pathways and reprobed for β-actin. RNAs were assayed for miR193a. In vivo studies, renal tissues of 4-week old control and HIV transgenic (Tg26) mice (n=6) were evaluated for the activation of mTOR and EMT pathways (Western blotting analysis and immuno-labeling of renal cortical sections). Renal tissues from control and Tg26 mice were also examined for miR193a expression (Fluorescent in situ hybridization, FISH).


PECHIV stimulated PEC proliferation at lower concentrations (103 and 102 GEU/ml). PECHIVs-overexpressing miR193a exhibited a decrease in proliferation when compared to PECHIVs. PECHIVs and renal tissues from Tg26 mice showed the activation of the mTOR as well as EMT pathways. Renal cortical sections of Tg26 mice showed a decrease in miR193a expression when compared to control mice; additionally, renal cortical sections of Tg26 mice displayed enhanced proliferation of PECs as indicated by an increased number PCNA +ve cells in Bowman's space.


HIV induces PEC proliferation through down-regulation of miR193a.


  • NIDDK Support