Deficiency in nucleotide excision repair (NER) family gene activity is associated with non-pigmented hair fiber growth
The regulation of melanogenesis and the growth and pigmentation of hair fibers are affected by numerous intrinsic factors including general metabolism and nutritional status, hair-cycle dependent changes, body location, racial and gender differences, hormone-responsiveness, genetic defects and age-associated changes. The hair follicle bulb (HB) is the only site of pigment production for the hair shaft and melanogenically active melanocytes are located in the upper hair matrix (UH). We conducted a microarray study to discover gene expression patterns unique to non- pigmented hair follicle (HF) that may be implicated in the lack of melanogenesis in gray hair. Pigmented and non-pigmented HFs (n=10-20 per group) collected from the same individuals (n=6) were micro-dissected and transected into the lower one third and hair bulb and upper, non-bulbar, hair matrix and sheaths including the bulge region. Microarray data was verified with qPCR and immunohistochemistry. In comparison to pigmented upper hair matrix and HBs, several nucleotide excision repair (NER) family genes exhibited statistically significantly lower expression both in non- pigmented upper hair matrix and non- pigmented HB. These genes were identified as ERCC1, ERCC2, ERCC3, ERCC4, ERCC5, ERCC6, XPA, NTPBP, HCNP, DDB2 and POLH. Immunohistochemistry showed consistent results. Our results suggest that losing NER gene function may be consistent with DNA damage accumulation in melanocytes and a lack of melanin production in gray hair follicles. These results offer a new insight into the molecular changes that occur in non- pigmented HF and may also provide novel information with regard to the importance of melanogenesis.