Scientists ID Scar Formation Mechanism

CHICAGO, June 15 (UPI) — U.S. biologists say they’ve discovered an unexpected cellular response plays a major role in the formation of excess scar tissue in wound healing.

The researchers, led by University of Illinois-Chicago Professor Lester Lau, said when an organism suffers severe injury, specialized cells are “recruited” to the wound site and rapidly produce extracellular matrix proteins — such as collagen — to provide structural support to the tissue.


In the study, Lau and postdoctoral fellow Joon-Il Jun, first author of the research, found fibroblasts recruited to the site of skin wounds were entering a state of reproductive dormancy, or cell-cycle arrest, called senescence. Jun said that was unexpected, because senescence was believed to occur in cells that suffered DNA damage — to prevent them from proliferating and possibly becoming cancerous.

The scientists said they also found the fibroblasts not only were making proteins that accelerated the breakdown of collagen, they also stopped making collagen.

“The accumulation of senescent cells in the wound has the biological effect of inhibiting the formation of excess scar tissue,” Jun said.

Lau said the study’s findings might prove important in understanding a wide range of pathological conditions related to tissue scarring, including organ damage where functional tissue is replaced with scar tissue.

The study appears in the early online edition of the journal Nature Cell Biology.

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