Estrogen Leads to Reversible Hair Cycle Retardation through Inducing Premature Catagen and Maintaining Telogen
نویسندگان
چکیده
Estrogen dysregulation causes hair disorder. Clinical observations have demonstrated that estrogen raises the telogen/anagen ratio and inhibits hair shaft elongation of female scalp hair follicles. In spite of these clinical insights, the properties of estrogen on hair follicles are poorly dissected. In the present study, we show that estrogen induced apoptosis of precortex cells and caused premature catagen by up-regulation of TGF β2. Immediately after the premature catagen, the expression of anagen chalone BMP4 increased. The up-regulation of BMP4 may further function to prevent anagen transition and maintain telogen. Interestingly, the hair follicle stem cell niche was not destructed during these drastic structural changes caused by estrogen. Additionally, dermal papilla cells, the estrogen target cells in hair follicles, kept their signature gene expressions as well as their hair inductive potential after estrogen treatment. Retention of the characteristics of both hair follicle stem cells and dermal papilla cells determined the reversibility of the hair cycle suppression. These results indicated that estrogen causes reversible hair cycle retardation by inducing premature catagen and maintaining telogen.
منابع مشابه
Roles of GasderminA3 in catagen- telogen transition during hair cycling
Hair follicles undergo cyclic behavior through regression (catagen), rest (telogen), and regeneration (anagen) during postnatal life. The hair cycle transition is strictly regulated by the autonomous and extrinsic molecular environment. However, whether there is a switch controlling catagen-telogen transition remains largely unknown. Here we show that hair follicles cycle from catagen to the ne...
متن کاملExpression of E6 and E7 papillomavirus oncogenes in the outer root sheath of hair follicles extends the growth phase and bypasses resting at telogen.
Hair follicle growth cycle proceeds through a series of stages in which strict control of cell proliferation, differentiation, and cell death occurs. Transgenic mice expressing human papillomavirus type 16 E6/E7 papillomavirus oncogenes in the outer root sheath (ORS) display a fur phenotype characterized by lower hair density and the ability to regenerate hair much faster than wild-type mice. R...
متن کاملIdentification of novel telogen markers underscores that telogen is far from a quiescent hair cycle phase
In contrast to the dynamic and striking changes in hair follicle (HF) morphology during the anagen and catagen phases of the hair cycle, the telogen follicle appears static. However, it has been argued that the quiescent appearance of telogen HFs is deceptive (Davis 1962, Stenn, Paus 2001, Higgins, Westgate 2009). For example, the expression of some genes clearly peaks during telogen (Greco, Ch...
متن کاملThe effect of parathyroid hormones on hair follicle physiology: implications for treatment of chemotherapy-induced alopecia.
Parathyroid hormone (PTH) and parathyroid hormone-related protein (PTHrP) influence hair follicles through paracrine and intracrine routes. There is significant evidence that PTH and PTHrP influence the proliferation and differentiation of hair follicle cells. The PTH/PTHrP receptor signalling plays an important role in the hair follicle cycle and may induce premature catagen-telogen transition...
متن کاملExpression of matrix metalloproteinases and tissue inhibitor of matrix metalloproteinases in the hair cycle
According to the growth state of hair follicles, the hair cycle is divided into the anagen, catagen and telogen phases. A number of biological factors have been shown to synchronize with the hair cycle. As an important component of the hair follicle, the extracellular matrix is regulated by matrix metalloproteinases (MMPs) and their inhibitors (tissue inhibitor of matrix metalloproteinases; TIM...
متن کامل