机构地区:[1]Department of Dermatology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210029, China [2]Department of Microbiology and Immunology, Nanjing Medical University, Nanjing, Jiangsu 210029, China
出 处:《The Journal of Biomedical Research》2012年第5期372-380,共9页生物医学研究杂志(英文版)
基 金:supported by grants from the National Natural Science Foundation of China(No.30571678 and No.30771947);the Natural Science Foundation of Jiangsu Province(No.BK2007248)
摘 要:Hypertrichosis is one of the most common side effects of systemic cyclosporine A therapy.It has been previously shown that cyclosporine A induces anagen and inhibits catagen development in mice.In the present study,to explore the mechanisms of cyclosporine A,we investigated the effects of cyclosporine A on hair shaft elongation,hair follicle cell proliferation,apoptosis,and mRNA expression of selected growth factors using an organ culture model of mouse vibrissae.In this model,cyclosporine A stimulated hair growth of normal mouse vibrissae follicles by inhibiting catagen-like development and promoting matrix cell proliferation.In addition,cyclosporine A caused an increase in the expression of vascular endothelial growth factor(VEGF),hepatocyte growth factor(HGF),and nerve growth factor(NGF),and inhibited follistatin expression.Our findings provide an explanation for the clinically observed effects of cyclosporine A on hair growth.The mouse vibrissae organ culture offers an attractive model for identifying factors involved in the modulation of hair growth.Hypertrichosis is one of the most common side effects of systemic cyclosporine A therapy.It has been previously shown that cyclosporine A induces anagen and inhibits catagen development in mice.In the present study,to explore the mechanisms of cyclosporine A,we investigated the effects of cyclosporine A on hair shaft elongation,hair follicle cell proliferation,apoptosis,and mRNA expression of selected growth factors using an organ culture model of mouse vibrissae.In this model,cyclosporine A stimulated hair growth of normal mouse vibrissae follicles by inhibiting catagen-like development and promoting matrix cell proliferation.In addition,cyclosporine A caused an increase in the expression of vascular endothelial growth factor(VEGF),hepatocyte growth factor(HGF),and nerve growth factor(NGF),and inhibited follistatin expression.Our findings provide an explanation for the clinically observed effects of cyclosporine A on hair growth.The mouse vibrissae organ culture offers an attractive model for identifying factors involved in the modulation of hair growth.
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