Wound healing is a complex process that progresses in stages and for which there are few targeted treatments for when it goes wrong. Now, a new study has discovered how a small molecule that regulates gene expression plays a key role in progressing wounds through their healing stages.

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The researchers suggest the molecule they identified could be a new target for treating chronic wounds.

Chronic wounds affect between 0.2 and 1% of people in developed countries and represent a growing health concern and cost to society.

Current treatments concentrate on controllable factors such as clearing infections. The researchers behind the new study note there is a pressing need for treatments that go further than this and target the wound healing process itself.

The researchers suggest the molecule they identified – called miR-132 – could be a target for new treatments for wounds that are hard to treat.

In the Journal of Clinical Investigation, they describe how they focused on two of the stages of wound healing: the inflammatory and the proliferative. During the inflammatory stage, immune cells clear away debris such as damaged and dead cells and bacteria.

During the proliferative stage, skin cells multiply to grow new tissue. The transition to this stage from the inflammatory stage is a critical one and can decide whether the wound heals successfully or not.

Following on from previous work, the researchers investigated a group of molecules called microRNAs (abbreviated miRNAs) – small pieces of genetic code that do not hold instructions for making proteins, but regulate the genes that do.

They collected skin biopsies from the edge of wounds and looked for changes in miRNA expression during the healing process.

The team found that one miRNA in particular – called miR-132 – was very active during the inflammatory stage in a type of skin cell called epidermal keratinocytes, which form the outermost layer of the skin. They also noticed how the molecule peaked in the subsequent proliferative stage.

During the inflammatory stage, miR-132 caused fewer immune cells to move to the wound. Conversely, a lack of miR-132 caused more immune cells to move to the wound and increase inflammation.

During the proliferative stage, miR-132 promoted keratinocyte growth, while a lack of it held back cell growth and slowed wound healing.

Principal investigator, Ning Xu Landén, an assistant professor in the department of medicine at Karolinska Institutet in Stockholm, Sweden, says:

Our results show that miR-132 is important during the transition from the inflammatory to the proliferative phase and therefore acts as a critical regulator of skin wound healing.

Due to its pro-healing capacity, miR-132 may be an attractive therapeutic target for chronic skin wounds. Our goal is to develop a microRNA-based treatment to promote healing.”

Meanwhile, another team is working on a way to use nanoparticles to hasten wound healing. A study that Medical News Today reported in March 2015, explains how the experimental therapy – which uses nanoparticles to deliver an enzyme blocker – cut wound healing time by 50% in mice.

The researchers – from the Albert Einstein College of Medicine of Yeshiva University, Bronx, NY – hope their treatment will one day help patients with all kinds of wounds, from surgical incisions to diabetic ulcers.