JCI paper shows that loss of p21Cip1 increases production of SDF-1, which attracts inflammatory cells.
NIH researchers found that the protein p21Cip1 is involved in controlling the repair of damaged blood vessels in mice. As this repair seems to go awry in atherosclerosis, the investigators suggest that p21Cip1 plays a pivotal role in the development of this disease.
The repair of a damaged blood vessel involves both cells that reside in the blood vessel wall and inflammatory cells that infiltrate the blood vessel wall after it has been damaged.
Researchers discovered that the repair of damaged arteries was defective in mice lacking the protein p21Cip1. Specifically, smooth muscle cells residing in the wall of the artery were found to proliferate excessively and the number of inflammatory cells infiltrating the wall of the damaged artery was markedly greater than in normal mice.
These effects were associated with increased production by cells in the artery wall of the soluble factor SDF-1, which attracts inflammatory cells. Further analysis indicated that p21Cip1 inhibits a signaling molecule important for inducing SDF-1 production.
The study was published May 8 in the Journal of Clinical Investigation.
