Keloid is an abnormal scar that often develops in high-tension skin. It is caused by excessive fibroblast proliferation and collagen deposition. Non-muscle myosin IIA (NM-IIA) is an important motor protein that regulates the mechanical transduction of cells.

A new study published in Advances in Wound Care aimed to ascertain the role of NM-IIA in keloid pathogenesis.

In this study, NM-IIA expression was examined and compared in keloid skin and normal skin by immunofluorescence. The organization of smooth muscle actin (SMA)-mediated stress fibers in normal and keloid fibroblasts (NFs and KFs, respectively) were determined. Cell proliferation and cell contractility were measured in fibroblasts derived from normal and keloids. The NM-II pharmacological inhibitor – blebbistatin, and RNA interference were applied to block NM-IIA and investigate its regulatory role in SMA-mediated stress fibers, cell contractility and cell proliferation after NM-IIA inhibition.

The results showed that the NM-IIA expression is increased in keloid tissue. Inhibition of NM-II by blebbistatin or targeting NM-IIA by RNA interference reduced transforming growth factor beta (TGF-β)-mediated SMA-mediated stress fiber formation, cell proliferation and cell contractility of NFs and KFs. Although TGF-β failed to mediate phosphorylation of myosin light chain—pMLC, the activator of NM-II—pMLC can interact with SMA-mediated stress fiber. Furthermore, the inhibition of NM-II by blebbistatin also reduced NF and KF proliferation after TGF-β stimulation.

Thus,NM-IIA synergizes with TGF-β to regulate fibroblast proliferation, contraction activity, and myofibroblasts differentiation. The findings suggested that NM-IIA might be one of the therapeutic targets in keloids.

Source: Advances in Wound Care. 2020 Sep;9(9):491-501. doi: 10.1089/wound.2019.0944. Epub 2020 Jan 14.