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Fewer mitochondria depolarize (green) in control cells (top) than in cells lacking prohibitin-1 (bottom).

During angiogenesis, the protein prohibitin-1 doesn't live up to its name. Instead of stopping some cellular process, it encourages new blood vessel growth by ensuring that mitochondria run efficiently, as Schleicher et al. reveal.

For lower organisms, prohibitin-1 is an asset. It keeps mitochondria functioning smoothly, and its loss pushes cells into the low-activity, slow-dividing state called senescence. The researchers suspected that prohibitin-1 would do a similar job in mammals and might be particularly important for vascular homeostasis, since mitochondrial maintenance is known to be important for vascular health—reactive oxygen species (ROS) that spill out from malfunctioning mitochondria can damage endothelial cells and prompt atherosclerosis.

The team knocked down the protein in mammalian endothelial cells and found that the cells' ROS levels shot up and several signs of senescence became apparent. Without the protein, cells also moved less and wouldn't roll up into tubes, suggesting that angiogenesis as well as homeostasis was affected.

To gauge prohibitin-1's effects on angiogenesis in vivo, the team injected mice with small amounts of a gel that contains the blood vessel growth promoter VEGF. Endothelial cells swarmed into the gel—unless it also contained RNAi that blocks prohibitin-1. The rapid increase in ROS following prohibitin-1 loss was caused by depolarization of the mitochondria membranes, suggesting that prohibitin-1 somehow maintains membrane integrity.

Reference:

Schleicher, M., et al. 2008. J. Cell Biol. 180:101–112.[Abstract/Free Full Text]

Mitch Leslie

mitchleslie{at}comcast.net

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This Article PDF (Full Text) Alert me when this article is cited Services Email this article Similar articles in this journal Alert me to new content in the JCB Download to citation manager Citing Articles Citing Articles via CrossRef Google Scholar Articles by Leslie, M. PubMed Articles by Leslie, M. Social Bookmarking                      What's this?