Cyclophilin A as negative regulator of apoptosis by sequestering cytochrome c

Biochem Biophys Res Commun. 2010 Mar 5;393(2):325-30. doi: 10.1016/j.bbrc.2010.01.135. Epub 2010 Feb 6.

Abstract

The release of cytochrome c from the mitochondrial intermembrane space is a decisive event in programmed cell death. Once in the cytoplasm, cytochrome c is involved in the formation of the macromolecular complex termed apoptosome, which activates procaspase-9 which in turn activates downstream procaspase-3. There are increasing evidence indicating that cyclophilin A is highly expressed in many tumors and cell lines where it exerts an anti-apoptotic function. In brain tissue, which over-expresses constitutively cyclophilin A, we found mixed dimers composed of cyclophilin A and cytochrome c. In a cell-free system we observed that pure cyclophilin A inhibited cytochrome c-dependent procaspase-3 activation. Moreover, we detected cyclophilin A-cytochrome c complexes within the cytoplasm of HCT116 cells following staurosporine-induced apoptosis. Our results strongly support that, in tumor cells, cyclophilin A is able to inhibit procaspase-3 activation by sequestering cytochrome c.

MeSH terms

  • Animals
  • Apoptosis*
  • Brain / enzymology*
  • Caspase Inhibitors
  • Cell Line, Tumor
  • Cyclophilin A / metabolism*
  • Cytochromes c / metabolism*
  • Humans
  • Neoplasms / enzymology*
  • Neurons / enzymology

Substances

  • Caspase Inhibitors
  • Cytochromes c
  • Cyclophilin A