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New Insights into Mechanisms Controlling Scar Formation

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Fibroblasts

New Insights into Mechanisms Controlling Scar Formation

July 08, 2010

By Hillary Hoffman for Scars1

A patient awaiting surgery and a patient getting stitches in the ER following a bike crash may ask the same question, “Will I have a scar?”  Understanding scar formation, also called fibrosis, could lead to new methods of scar prevention and treatment.

In order to repair a wound, the body recruits cells called fibroblasts to the site of the trauma.  Fibroblasts produce collagen, a protein that makes up an integral component of skin and gives the skin its firmness and elasticity.  Fibroblasts also synthesize components of the extracellular matrix, a complex structure that surrounds and supports cells.

A scar typically forms as the result of excess collagen production during wound repair. Hypertrophic scars and keloid scars, with their thick and raised appearance, are prime examples of this phenomenon.  Acne scars and some surgical scars are atrophic, which means that they result from a loss of tissue.  These skin depressions are formed when inflammation destroys collagen during the wound healing process.

Take Action

Have you recently cut or injured yourself?  Reduce the risk of scarring by:

  • Treating your wound well.  Keep it lightly covered and clean it daily with antibacterial soap.
  • Massaging the injured area after the wound has closed up.  This may help break up some of the dense collagen that forms.
  • Avoiding the sun; sun exposure can slow down healing.
  • Considering topical application of aloe vera.
  • Paying attention to your overall health.  Don't smoke.  Make sure you eat well.
  • Just a few weeks ago, researchers at the University of Illinois at Chicago made an important contribution to understanding the scar formation process.  Their research, which was published in Nature Cell Biology, provides insight into the mechanism that limits scar formation

    The publication reveals the unexpected finding that the fibroblasts recruited for wound repair enter a state called reproductive senescence.  Senescent cells are cells that can no longer divide.  The cells can remain metabolically active for some time, but the inability to reproduce is irreversible.  Certain cell types, including fibroblasts, are known to become senescent as a result of aging or DNA damage.  In the latter case, senescence functions as a protective mechanism by keeping the damaged cells from multiplying and possibly becoming cancerous.

    In addition to uncovering the role of senescence in wound healing, the researchers pinpointed the switch responsible for turning on the senescent state – a protein called CCN1 that is known to be involved in cell adhesion, proliferation, and differentiation. 

    In wound healing, CCN1 binds to receptors involved in cell adhesion and induces DNA damage response pathways.  This sets off a complex cellular signaling cascade that results in senescence and production of anti-fibrotic proteins, which help prevent scarring.  The senescent fibroblasts stop producing new collagen and start making proteins that degrade the extracellular matrix and break down collagen.

    The importance of CCN1 was established by experiments with mutant mice possessing a non-functional form of CCN1.  When wounded, these mice developed excessive scar tissue.  However, the effects could be reversed by topical application of CCN1.

    This new study sheds valuable light on the scar formation process and its control mechanisms.  Understanding the scarring process is relevant not only to skin wounds but also to internal wounds, such as liver damage resulting from viral infections or chronic alcoholism and cardiac scar tissue that forms in the aftermath of a heart attack.

    Scientists are also excited about the potential therapeutic applications.  If they can devise a way to control fibrosis, they could limit scar formation and treat wound-healing disorders.     

    Discuss in the Scars1 forums.  

    Sources and Related Links

    Press release: Researchers discover mechanism that limits scar formation

    Joon-Il Jun, Lester F. Lau. The matricellular protein CCN1 induces fibroblast senescence and restricts fibrosis in cutaneous wound healing. Nature Cell Biology, 2010 [PubMed abstract]

    Cellular senescence overview

    Photo credit: GE Healthcare

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