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Healing skin from within

Wounds cause more damage from oxidative stress (pink) in mice lacking peroxiredoxin 6 (right).

Forget about those age-defying face creams and moisturizing lotions. The real savior of our skin is the enzyme peroxiredoxin 6 (Prdx6). As Kümin et al. report, the oxidant-fighting enzyme spares skin cells damaged by UV radiation and protects new blood vessels during wound healing.

In vitro, Prdx6 neutralizes damaging reactive oxygen species (ROS). But scientists are just beginning to tease out its functions in vivo. Last year, the researchers found that rodents that overproduce Prdx6 in the skin suffer less damage from UV radiation. Moreover, the extra enzyme accelerates wound healing in aged animals, which are slow to mend. These results make sense, since sunburns induce ROS, and the inflammatory cells that arrive at an injury also spill the destructive molecules.

To further probe the enzyme's protective powers, the team gave Prdx6-deficient mice sunburns. The animals' keratinocytes, which normally divide rapidly to help restore the scorched skin, killed themselves in droves, suggesting that one of Prdx6's jobs is preventing damage to—and subsequent death of—repair cells. When the researchers sliced out patches of the rodents' skin, severe hemorrhages resulted. The new blood vessels sprouting into the cuts were flimsy because many of their endothelial cells were damaged or had committed suicide, the team found.

Vessel damage might occur because endothelial cells in Prdx6-deficient rodents can't fend off ROS or because inflammatory cells can't neutralize their own ROS, which then seep into the surrounding tissue. To test these alternatives, the researchers performed bone marrow transplants on normal mice and rodents lacking Prdx6.

Hemorrhages occurred when the recipient and the transferred cells were missing the enzyme. But some bleeding resulted when either the recipient animal or the implanted cells lacked Prdx6. Those results indicate that vessel weakness stems from lowered defenses in endothelial cells and from self-inflicted damage caused by ROS leakage from inflammatory cells. The findings also suggest that Prdx6 activators might help protect our skin from sun damage and even stave off skin cancer.

Reference:

Kümin, A., et al. 2007. J. Cell Biol. 179:747–760.[Abstract/Free Full Text]

Mitch Leslie

mitchleslie{at}comcast.net

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This Article Full Text (PDF, 1420K) PPT slides of all figures 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 Citing Articles via Google Scholar Google Scholar Articles by Leslie, M. Search for Related Content PubMed Articles by Leslie, M. Social Bookmarking                            What's this?