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References: Hair growth and hair loss







J Invest Dermatol. 2004 Jan;122(1):7-13.
Topical estrogen accelerates hair regrowth in mice after chemotherapy-induced alopecia by favoring the dystrophic catagen response pathway to damage.

Ohnemus U, Unalan M, Handjiski B, Paus R.

Department of Dermatology, University Hospital Hamburg-Eppendorf, University of Hamburg, Hamburg, Germany.

Estrogen receptor ligands are important modulators of skin physiology and are involved in the control of normal hair follicle cycling. Here, we have studied the effects of topically applied 17-beta-estradiol on pathologic hair follicle cycling as seen during chemotherapy-induced alopecia, one of the major unresolved problems of clinical oncology. For this study we employed a well-established murine model that mimics chemotherapy-induced alopecia in humans. For precisely quantifying the area of hair loss and hair regrowth in this model in vivo, we developed a simple planimetric assay (dotmatrix planimetry). We show that topical 17-beta-estradiol significantly alters the cycling response of murine follicles to cyclophosphamide, whereas the estrogen antagonist ICI 182.780 exerted no such effects. Initially, topical 17-beta-estradiol enhanced chemotherapy-induced alopecia significantly by forcing the follicles into the dystrophic catagen response pathway to hair follicle damage, whereas follicles treated by ICI 182.780 or vehicle shifted into the dystrophic anagen response pathway. Consequently, the regrowth of normally pigmented hair shafts after chemotherapy-induced alopecia was significantly accelerated in the 17-beta-estradiol treated group. Our data encourage one to explore topical estrogens as a potential stimulant for hair re-growth after chemotherapy-induced alopecia.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=14962083&dopt=Abstract




Br J Dermatol. 1992 Feb;126(2):166-71.
Failure of passive transfer of serum from patients with alopecia areata and alopecia universalis to inhibit hair growth in transplants of human scalp skin grafted on to nude mice.

Gilhar A, Pillar T, Assay B, David M.

Skin Research Laboratory, Bruce Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa.

We have previously demonstrated regrowth of hair in scalp skin grafts taken from patients with alopecia areata (AA) and alopecia universalis (AU) following engraftment on to nude mice. This present study was to determine whether serum from patients with AA and AU, has a role in the process of hair loss and the role of antibodies and complement. Forty mice were grafted with transplants obtained from seven patients. One group of the grafted mice was given patients' serum and another group normal serum. The mice were treated topically with cyclosporin (CyA), or olive oil. Hair growth was noted in most grafts and intravenous injections of serum did not prevent or inhibit this process. Immunofluorescence studies before grafting showed deposition of immunoglobulins and complement in hair follicles in both normal and affected scalp skin, but a more striking deposition was noted in the affected skin. Deposition of immunoreactants after grafting was observed only after the injection of serum from the patients but not with normal serum. Thus the sera from patients with AA or AU, when injected into nude mice with hair transplants from the scalp skin of patients with these disorders, does not alter the hair growth despite deposition of immunoreactants around the hair follicles.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1536782&dopt=Abstract




J Invest Dermatol. 1992 May;98(5):734-40.
Comparison of the effect of 8-methoxypsoralen (8-MOP) plus UVA (PUVA) on human melanocytes in vitiligo vulgaris and in vitro.

Kao CH, Yu HS.

Department of Dermatology, Kaohsiung Medical College, Taiwan, Republic of China.

In this study, we examined the various effects of PUVA treatment on cultured human melanocytes, and it revealed that 1) the higher the dose of PUVA treatment, the more significant the inhibition of cell DNA and protein synthesis; 2) the higher the dose of PUVA treatment, the more significant the depletion of epidermal growth factor receptor (EGFR) expression; 3) PUVA treatment at 124 mJoule/cm2 depleted the vitiligo-associated melanocyte antigens (VAMA) immediately after irradiation, and both the VAMA and EGFR expression progressively recovered at 24 or 72 h after PUVA; 4) PUVA treatment stimulated tyrosinase activity, but not in a dose-dependent fashion. In vitiligo vulgaris, PUVA treatment may stimulate the regrowth of melanocytes from hair follicles, but deplete the epidermal Langerhans cells in depigmented lesion of patients with stable vitiligo. Comparing the above results obtained from in vivo and in vitro studies, it reveals significantly different biologic responses. Although the precise therapeutic mechanism of PUVA treatment in vitiligo is still not well known, it is proposed that 1) PUVA treatment may stimulate the other components of skin, such as keratinocytes, to release inflammatory mediators and some of them may act as melanocyte growth-stimulatory factors (MGSF), which further enhance the proliferation of remaining melanocytes in hair follicle; and 2) PUVA treatment may deplete the VAMA expression on cell membrane of melanocytes and also deplete epidermal Langerhans cells, which may result in blocking the progressing of antibody-dependent cell-mediated cytotoxicity to melanocytes in vitiligo.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1569322&dopt=Abstract





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