Anti-mouse mesangial cell serum induces acute glomerulonephropathy in mice.

Yoshikage Yo, Michael C. Braun, Laura Barisoni, Hideko Mobaraki, Huiyan Lu, Shashi Shrivastav, Jennie Owens, Jeffrey B. Kopp

Research output: Contribution to journalArticlepeer-review

12 Scopus citations

Abstract

In order to develop a model in mouse similar to anti- Thy-1 nephritis in the rat, we prepared sheep antiserum against SV40-transformed mouse mesangial (MES 13) cells. In vivo, the anti-mouse mesangial cell serum-treated mice showed severe azotemia that peaked at day 6 and proteinuria that peaked at day 8, in a dose-dependent fashion. Light microscopy and electron microscopy showed duplication of glomerular basement membranes, mesangiolysis, subendothelial and mesangial electron-dense deposits, and foot process effacement. Intraglomerular tuft cell number was significantly reduced at day 4 and there were increased numbers of apoptotic cells at days 2 and 4. SCID mice and mice lacking C3 manifested similar responses to anti-mouse mesangial cell serum, suggesting that T cells, B cells and complement are not required for glomerular injury in this model. In vitro, anti-mouse mesangial cell serum treated mesangial cells showed greater release of lactate dehydrogenase, decreased cell survival, and increased apoptotic cell death. Anti-mouse mesangial cell serum induces glomerulopathy characterized by mesangiolysis and mesangial cell apoptosis, and followed by cellular proliferation.

Original languageEnglish (US)
Pages (from-to)e92-106
JournalNephron. Experimental nephrology
Volume93
Issue number3
DOIs
StatePublished - 2003
Externally publishedYes

ASJC Scopus subject areas

  • Physiology
  • Genetics
  • Nephrology

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