Abstract. The precise mechanisms of alopecia, a pathophysiological disorder with negative psychological implications, are unknown. Androgen and hereditary predisposition are major causes, but the condition is also affected by stress, an irregular diet and high levels of sebum secretion. We focused on oxidative stress and analyzed the effect of the lipid peroxides on hair follicles. Our first observation was that the topical application of linolein hydroperoxides, one of the lipid peroxides, lead to the early onset of the catagen phase in murine hair cycles. Furthermore, by using TUNEL staining we found that lipid peroxides induced apoptosis of hair follicle cells. They also induced apoptosis in human epidermal keratinocytes by up-regulating apoptosis-related genes. These results indicated that lipid peroxides, which can cause free radicals, induce the apoptosis of hair follicle cells, and this is followed by early onset of the catagen phase. These observations may provide insight into the mechanisms underlying the development of alopecia in humans.
One or both of two putative N-glycosylation sites (at asparagine-5 and -75) of human renin was eliminated by amino acid replacement of the asparagine residue with an alanine residue using site-directed mutagenesis. The three glycosylation-deficient renins (Asn-5, Asn-75, Asn-5 and -75 mutants) were expressed in COS cells and secreted into the conditioned media. The secreted amounts of the three mutants were different from one another, although the mutant and wildtype renins had practically the same specific activity. An Asn-5 and -75 mutant which did not contain any glycosylation sites was unstable in the medium, suggesting that the N-linked oligosaccharides play an important role in stabilization of human renin.
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