new hair from sides put on top full of dht and grow for life how come ??????

CRF Receptor Antagonist Astressin-B Reverses and Prevents Alopecia in CRF Over-Expressing Mice

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Abstract
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Results
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Lixin Wang1#, Mulugeta Million1#*, Jean Rivier2, Catherine Rivier2, Noah Craft3, Mary P. Stenzel-Poore4, Yvette Taché1

1 Division of Digestive Diseases, Department of Medicine, CURE and Center for Neurobiological Stress, David Geffen School of Medicine at University of California Los Angeles, VA Greater Los Angeles Healthcare System, Los Angeles, California, United States of America, 2 Clayton Foundation Laboratories for Peptide Biology, Salk Institute for Biological Studies, San Diego, California, United States of America, 3 Divisions of Dermatology and Infectious Diseases, Department of Medicine, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, David Geffen School of Medicine at University of California Los Angeles, Torrance, California, United States of America, 4 Department of Molecular Microbiology and Immunology, Oregon Health & Sciences University, Portland, Oregon, United States of America
Abstract Top

Corticotropin-releasing factor (CRF) signaling pathways are involved in the stress response, and there is growing evidence supporting hair growth inhibition of murine hair follicle in vivo upon stress exposure. We investigated whether the blockade of CRF receptors influences the development of hair loss in CRF over-expressing (OE)-mice that display phenotypes of Cushing's syndrome and chronic stress, including alopecia. The non-selective CRF receptors antagonist, astressin-B (5 µg/mouse) injected peripherally once a day for 5 days in 4–9 months old CRF-OE alopecic mice induced pigmentation and hair re-growth that was largely retained for over 4 months. In young CRF-OE mice, astressin-B prevented the development of alopecia that occurred in saline-treated mice. Histological examination indicated that alopecic CRF-OE mice had hair follicle atrophy and that astressin-B revived the hair follicle from the telogen to anagen phase. However, astressin-B did not show any effect on the elevated plasma corticosterone levels and the increased weights of adrenal glands and visceral fat in CRF-OE mice. The selective CRF2 receptor antagonist, astressin2-B had moderate effect on pigmentation, but not on hair re-growth. The commercial drug for alopecia, minoxidil only showed partial effect on hair re-growth. These data support the existence of a key molecular switching mechanism triggered by blocking peripheral CRF receptors with an antagonist to reset hair growth in a mouse model of alopecia associated with chronic stress.