Researchers of Kerala University have evolved a solution to limit the impact of primary cicatricial alopecia (PCA), a rare hair loss disorder, by controlling cholesterol production in hair cells.
A study conducted by the Zoology department and the Advanced Centre for Regenerative Medicine and Stem Cell Research Centre in Cutaneous Biology (AcREM-Stem) in the university has found that accelerating the production of cholesterol in hair follicles and reducing inflammation could prevent abnormal hair loss caused by PCA.
The research, which was recently published in the Journal of Endocrinology and Reproduction, was undertaken by a team supervised by assistant professor P. Sreejith of the Zoology department. It comprised Nikhila Leemon, Surya Suresh, Binumon T.M., and Najeeb S.
Damages hair follicles
Ms. Leemon, the lead author, points out that the hair follicles of those affected by PCA, which is an autoimmune condition that affected the skin, are irreversibly damaged and replaced with fibrous tissue. Fibrosis, itching and pain are the pathophysiological trademarks of alopecia. The difficulty in differentiating many of the diseased conditions as well as the overlap in clinical and histological findings are the major clinical and treatment problems associated with the condition.
The research team had earlier found that the inhibition of cholesterol biosynthesis causes permanent damage to hair follicles by promoting fibrosis (or scarring). It also suggested that an altered cholesterol biosynthetic pathway led to the functional elevation of the inflammatory pathway, which acts as a positive regulator of tissue fibrosis in PCA.
Its latest study focused on how epithelial mesenchymal transition (EMT), the process that causes fibrosis in the body, is accelerated by disruptions in cholesterol production in hair follicles. The researchers altered the cholesterol biosynthetic pathway using two compounds – 7DHC (a cholesterol precursor) and BM15766 (a pharmacological inhibitor). These compounds were treated in vitro (human hair follicle outer root sheath) and in vivo (in mice) model systems. It was observed that the inflammation caused by PCA could be decreased by activating cholesterol biosynthesis.
