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Identified 'switch' molecular critical for wound healing

Discovery opens door to new therapies to improve the healing of chronic wounds, especially in diabetic patients

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Researchers from A * STAR's Institute of Medical Biology (IMB) in Singapore, identified a critical molecular switch for wound healing.

The discovery opens the way for new therapies to improve healing of chronic wounds such as those that occur in diabetic patients.

Scientists have found that a small molecule "microRNA", called miR-198, controlling several different processes that assist wound healing by keeping them off the skin healthy. When skin is wounded, manufacturing miR-198 is stopped rapidly and levels fall miR-198, connecting the processes of healing many wounds.

Wounds that do not heal diabetic, miR-198 does not disappear and healing remains blocked. This finding therefore identified miR-198 as a potential biomarker for diagnosis of wounds that do not heal.

The results were published in Nature.

Chronic wounds in patients with diabetes are a major global health problem and the most common cause of lower limb amputations. In Singapore, diabetes is the fifth most commonly diagnosed medical condition and one in nine people between 18 and 69 have diabetes. Chronic wounds also tend to affect the elderly and people with disabilities, especially those confined to a wheelchair or bed.

According to the researchers, the information necessary to express miR-198, and protein follistatin-like 1 (FSTL1) is found in a "message" produced by single cell. However, miR-198 and FSTL1 protein may not be produced simultaneously. These two molecules also have opposing roles: miR-198 (found in unwounded skin) inhibits migration of skin cells and wound healing, while FSTL1 (expressed after injury) promotes cell migration and healing of skin wounds.

A molecular switch said expression and, therefore, controls the "seesaw" inactive cells between the skin and migration of cells necessary for wound healing.

Lead researcher Prabha Sampath and his team showed that the uninjured healthy skin contained high levels of miR-198, but not protein FSTL1. They demonstrated that these high levels of miR-198 prevents the migration of skin cells, deleting several genes, as PLAU, and LAMC2 DIAPH1, which are required for the different aspects of the healing process of wounds. However the injury, miR-198 is wound off by a signal SS1 transforming growth factor (TGF-ß1). This allows FSTL1 now be produced, and the genes migration of the skin are released, promoting cell migration from the skin to the wound site leading to healing.

The scientists examined skin samples over chronic wounds in patients with diabetes mellitus. They noted that, unlike the healthy skin that had been wound, the skin of these individuals had elevated levels of miR-198 and the absence of FSTL1 protein, indicating that the "switch" is defective in chronic wounds.

Moving forward, we hope to translate this research into better outcomes for patients. We can now develop this research, to see how we can modulate the defective switch in chronic wounds, seeking as miR-198 and its molecules interact to develop new strategies for treating chronic wounds. Our research provides a comprehensive understanding of the mechanism of the process of wound healing, "concludes Sampath.

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