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Abstract: SA-PO356

Apolipoprotein L1 Dynamics in Human Parietal Epithelial Cell (PEC) Molecular Phenotype Kinetics

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
  • Marashi Shoshtari, Seyedeh Shadafarin, The Feinstein Institute for Medical Research, Manhasset, New York, United States
  • Chowdhary, Sheetal, Feinstein Institute of Medical Research, New Hyde Park, 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

PECs do not express APOL1. We hypothesize that APOL1 expression emerges in PECs for podocytes’ (PDs) renewal (PECs’ transition) in adverse milieus. We further hypothesize that the absence of APOL1 favors the PEC phenotype and that the induction of APOL1 transitions to PD renewal.


Immortalized human PECs, which proliferate at 33οC and differentiate (transition) after 14 days after incubation in special media were characterized and used. PECs’ expression of APOL1 was evaluated at different time intervals (0, 4, 8, 14 days) during their transition (Tr). Effects of a miR193a inhibitor/ overexpression of miR193a as well as APOL1-silencing/APOL1-overexpression was evaluated on PECs’ expression APOL1 and miR193a. Effects of vitamin D receptor agonist (VDA), IFN-y, and HIV were examined on the induction of APOL1 and associated expression of PD markers in HEKs and PECs. Luciferase assay was used to establish a putative interaction between miR193a and APOL1 in PECs. To confirm the PEC induction of APOL1 in vivo, renal biopsy specimens of HIVAN patients were co-labeled for APOL1 and synaptopodin.


PECs at 33οC did not exhibit APOL1 expression. During PECs’ transition, APOL1 expression coincided with the expression of PD markers (PEC transition) along with down-regulation of miR193a. The induction of APOL1 down-regulated miR193a and induced PD markers in PECs; whereas, the APOL1-silencing in Tr-PECs up- regulated miR193a expression suggesting a reciprocally linked feedback loop relationship between APOL1 and miR193a. HIV, IFN-γ, and VDA down-regulated miR193a expression as well as induced the expression of APOL1 and PD markers both in PECs. Since silencing of APOL1 attenuated HIV-, VDA-, and IFN-y-induced expression of PD makers, it appears that APOL1 is an important functional constituent of miR193a-APOL1 axis. This notion was further confirmed by enhanced expression of PEC markers in APOL1 silenced Tr-PECs despite down-regulation of miR193a. Luciferase assay suggested a putative interaction between miR-193a and APOL1. Renal biopsy specimens from HIVAN patients revealed PECs’ expression of APOL1 and synaptopodin.


APOL1 absence favors PECs’ phenotype but its expression facilitates PECs transition


  • NIDDK Support