Researchers discover mechanism that limits scar formation

June 12th, 2010 - 4:56 pm ICT by IANS  

Washington, June 12 (IANS) Researchers have discovered that an unexpected cellular response plays an important role in breaking down and inhibiting the formation of excess scar tissue in wound healing.
When an organism suffers severe injury, specialised cells are “recruited” to the wound site that rapidly produce extracellular matrix proteins such as collagen to provide structural support to the tissue, says Lester Lau, principal study investigator.

Lau is also professor of biochemistry and molecular biology at the University of Illinois-Chicago (UIC) College of Medicine.

Joon-Il Jun, postdoctoral fellow working in Lau’s lab and study co-author, found that fibroblasts recruited to the site of skin wounds were entering a state of reproductive dormancy, or cell-cycle arrest, called senescence.

(A fibroblast is a type of cell that synthesizes the extracellular matrix and collagen, the structural framework for animal tissues).

This was quite unexpected, Jun said. Until now senescence was believed to occur in cells that suffered DNA damage — to prevent them from proliferating and, possibly, becoming cancerous.

He discovered that the senescent fibroblasts were making proteins that degraded the extracellular matrix and accelerated the breakdown of collagen. The senescent cells 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.

Jun also discovered that a protein called CCN1 is responsible for turning on the senescent state in fibroblasts.

He was able to show that in mice with a mutated, non-functional form of CCN1, the fibroblasts at the site of a skin wound did not become senescent, and the wound developed excessive scar tissue, said an UIC release.

The ability to control the formation of scar tissue, or fibrosis, has important implications for future therapies for treating wound-healing disorders, including organ damage where functional tissue is replaced with scar tissue, Lau said.

Their study was published online this week in Nature Cell Biology.

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