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Study pinpoints protein that helps to regulate wound healing.

Wound repair is an important aspect of physiology, and disruption of this process can result in a number of defects involving wound healing, chronic ulceration and scarring.   A scar on a person’s skin may look bad, however, it can become life-threatening with a heart attack where a scar is formed on the heart.  Now, a study from researchers at Ohio State University has pinpointed the human gene which helps to regulate wound healing and control scarring.  The team state that their findings could help heal open wounds, decrease recovery time after surgery and reduce the spread of infections.  The study published in The Journal Of Biological Chemistry.

Earlier studies from the lab show that the protein, Mitsugumin 53 (MG53) encoded by the TRIM72 gene, is an essential component of the cell membrane repair machinery. All animals carry this gene and it’s almost identical no matter which species.  Even simple actions, like walking or typing, will cause injuries to the body. Usually this isn’t a problem because MG53, a muscle-specific TRIM family protein, can make repairs before there’s any serious harm.  Despite all this MG53 is a membrane repair gene whose role in wound healing has not been studied.  The current study shows the functional role of MG53 in the modulation of wound healing and scarring.

The current study utilised genetically engineered mice without the gene that makes MG53 to see what would happen without its healing capabilities.  Results show that the mice lacking MG53 had difficulty recovering from injury, because of their compromised repair capacity; their heart would not function well under stress conditions.

Data findings show that MG53 works in tandem with another protein called TGF Beta, a type of cytokine protein that also heals wounds, however, the healing process happens so quickly that it causes scars. The group state, therefore, if a person has more TGF Beta in their bloodstream than MG53, the person will scar easily.

The team surmise that their study establishes MG53 as facilitator of injury repair and inhibitor of myofibroblast differentiation during wound healing.  For the future, the researchers state that their goal is to develop a therapy that will inhibit TGF Beta and promote MG53. They go on to add that medical professionals can use the therapy during procedures to promote quick, scarless healing.

Source: The Biophysical Society Annual Meeting

 

This image shows modulation of wound healing and scar formation by MG53-mediated cell membrane repair and TGF-β signaling regulation. Credit: Li.et.al., 2015.
This image shows modulation of wound healing and scar formation by MG53-mediated cell membrane repair and TGF-β signaling regulation.
Credit: Li.et.al., 2015.

 

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