ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005


The Latest on X

Kidney Week

Please note that you are viewing an archived section from 2023 and some content may be unavailable. To unlock all content for 2023, please visit the archives.

Abstract: SA-PO836

Glomerular Parietal Epithelial Cell Expression of Cathepsin C Increases in Tg26 Mouse Model of HIV-Associated Nephropathy (HIVAN)

Session Information

Category: Glomerular Diseases

  • 1401 Glomerular Diseases: From Inflammation to Fibrosis


  • Barati, Michelle T., University of Louisville, Louisville, Kentucky, United States
  • Klein, Jon B., University of Louisville, Louisville, Kentucky, United States
  • Merchant, Michael, University of Louisville, Louisville, Kentucky, United States

Collapsing glomerulopathy (CG) is a feature of human immunodeficiency virus-associated nephropathy (HIVAN). Previous studies in kidney biopsies of patients with primary, collapsing variant of focal segmental glomerulosclerosis (cFSGS) demonstrated activated glomerular parietal epithelial cells (PEC) expressing cathepsin C protease, migrating into glomerular tufts. Similar results were found with preliminary lab studies in biopsies of HIVAN patients. Cathepsin C is normally absent in the glomerular tuft, suggesting that PEC introduction of this protease may contribute to extracellular matrix (ECM) remodeling in cFSGS. For this study, we addressed the hypothesis that cathepsin C expression increases in PECs lining Bowman’s capsule and PECs migrating onto glomerular tufts in Tg26 mouse model of HIVAN.


Kidneys from 8 week old male and female Tg26 transgenic and FVB wt mice used for this study were provided by Klotman lab, baylor college of medicine. Formalin-fixed paraffin-embedded kidney sections were subject to co-immunofluorescence staining for claudin-1, a marker of PECs, and cathepsin C. Images were acquired by confocal microscopy.


claudin-1 and cathepsin C were localized to glomerular parietal epithelial cells lining Bowman’s capsule in wt mice. In glomeruli of Tg26 mice, PECs lining Bowman’s capsule showed increased expression of cathepsin C and had hypertrophied morphology, suggesting PEC activation. Glomeruli of Tg26 mice also showed migration of Claudin-1-positive PECs onto the glomerular tuft and these cells also expressed cathepsin C.


Glomerular PECs exhibit increased expression of cathepsin C in Tg26 mouse model of HIVAN CG. These findings are similar to our findings from human primary cFSGS and HIVAN, demonstrating utility of this mouse model to define the role of PEC induction of cathepsin C in the pathogenesis of CG. Defining the cellular and molecular basis for abnormal ECM remodeling in cFSGS offers the potential of interrupting disease progression.