Cardiolipin induces premature senescence in normal human fibroblasts
P Arivazhagan, E Mizutani, M Fujii… - … and biophysical research …, 2004 - Elsevier
P Arivazhagan, E Mizutani, M Fujii, D Ayusawa
Biochemical and biophysical research communications, 2004•ElsevierLipids seem to have various roles in cellular senescence. We found that cardiolipin very
sensitively inhibits growth of normal human fibroblasts, whereas other phospholipids do not
at 100 times higher concentrations. Growth arrested cells showed morphology similar to
those of normally senesced cells and strongly induced senescence-associated β-
galactosidase. Senescence markers such as the p21waf1/sdi-1, fibronectin, and
collagenase-I genes were significantly upregulated by cardiolipin. In addition, caldiolipin …
sensitively inhibits growth of normal human fibroblasts, whereas other phospholipids do not
at 100 times higher concentrations. Growth arrested cells showed morphology similar to
those of normally senesced cells and strongly induced senescence-associated β-
galactosidase. Senescence markers such as the p21waf1/sdi-1, fibronectin, and
collagenase-I genes were significantly upregulated by cardiolipin. In addition, caldiolipin …
Lipids seem to have various roles in cellular senescence. We found that cardiolipin very sensitively inhibits growth of normal human fibroblasts, whereas other phospholipids do not at 100 times higher concentrations. Growth arrested cells showed morphology similar to those of normally senesced cells and strongly induced senescence-associated β-galactosidase. Senescence markers such as the p21waf1/sdi-1, fibronectin, and collagenase-I genes were significantly upregulated by cardiolipin. In addition, caldiolipin significantly increased in normally senesced human fibroblasts leaving other phospholipids unaltered. These results suggest that accumulation of cardiolipin is one of the causes for replicative senescence.
Elsevier
