Bcl-2 expression and apoptosis in nephrotoxic nephritis

Hitoshi Sugiyama, Naoki Kashihara, Tsuneto Onbe, Yasushi Yamasaki, Jim Wada, Takashi Sekikawa, Kazunori Okamoto, Koichiro Kanao, Yohei Maeshima, Hirofumi Makino

Research output: Contribution to journalArticlepeer-review

14 Citations (Scopus)


The product of the Bcl-2 proto-oncogene has been shown to prolong cell survival by preventing apoptosis in several cell lineages. To investigate the regulatory mechanisms of apoptosis in glomerulonephritis, we examined the expression pattern of the Bcl-2 protein together with cellular events in rat nephrotoxic nephritis. Bcl-2 protein and proliferating cell nuclear antigen were detected in glomeruli by immunohistochemistry. Morphologic changes of apoptosis were identified by electron and light microscopy and an in situ DNA nick end labeling method. The first (heterologous) phase began with significant neutrophil infiltration shortly after the injection of nephrotoxic serum. Both Bcl-2 expression and the number of proliferating cells in the glomeruli were at maximum at 24 h in the heterologous phase. Glomerular hypercellularity with an influx of macrophages and the number of apoptotic glomerular cells peaked on day 14 in the second (autologous) phase. Glomerulonephritis resolved after that. These results suggest that overexpression of the Bcl-2 protein may play a role in glomerular cell survival and exacerbation of glomerulonephritis. Apoptosis may occur as an active mechanism in the resolution of the autologous phase in nephrotoxic nephritis.

Original languageEnglish
Pages (from-to)481-489
Number of pages9
JournalExperimental Nephrology
Issue number6
Publication statusPublished - Nov 1 1997


  • Apoptosis
  • Autologous phase
  • Bcl-2
  • Heterologous phase
  • Inflammation
  • Masugi nephritis
  • Nephrotoxic serum

ASJC Scopus subject areas

  • Nephrology


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