Most of the latest http www apexbt com media diy

Most of the latest works reported that in human hair follicle AR expression is restricted to DPC and is not found in the outer root sheath (ORS), hair bulb or bulge (Itami et al., 1995a, Jave-Suarez et al., 2004, Kariya et al., 2005, Pelletier et al., 2004, Thornton et al., 2003). DPC derived from beard and balding scalp contain significantly greater levels of specific, low capacity, high affinity AR, as demonstrated with binding assays (Hibberts et al., 1998, Randall et al., 1992b), than those derived from relatively androgen-insensitive non-balding scalp follicles. This fact would suggest that androgens act on hair follicles via the dermal papilla in vivo reviewed in Inui and Itami (2011). Nevertheless, their expression in the ORS and medulla is controversial. Interestingly, AR mRNA was found to be expressed in dermal and epithelial portions of microdissected hair follicles from scalp (Asada et al., 2001). Moreover, type I hair keratin hHa7 and the AR are co-expressed in the medulla of male and female sexual hairs, and the expression of hHa7 appears to be directly regulated by androgens through three putative ARE motifs in its promoter (Jave-Suarez et al., 2004). Recently, the same group reported the in vitro androgenic regulation of this keratin in human occipital hair medulla, and a slight upregulation of AR expression in the nuclei of DPC and the bv8 of lower medulla of DHT-treated hair follicles (Yoshida et al., 2013). On the other hand, it was shown that TR3, an orphan member of the steroid/thyroid/retinoid nuclear receptor superfamily, is localized to the stem cell compartment in the human hair follicles. Furthermore, androgen increases TR3 expression in cultured keratinocytes, suggesting that TR3 mediates at least part of the inhibitory effect of androgens on keratinocytes (Xie et al., 2016).
Role of androgens in skin pathologies
Conclusions and perspectives
Conflict of interest
Acknowledgments
Introduction Spermatogenesis is under intricate hormonal regulation of the hypothalamo-pituitary-testis axis. Although pituitary hormones are master regulators of reproductive function, many vital functions are performed by locally secreted sex steroids such as androgens and estrogens, which are the final effector hormones. Estrogens signal mainly via their two cognate receptors estrogen receptor (ER) α and β, encoded by the ERα gene (Esr1) and the ERβ gene (Esr2), respectively, while androgens mediate their effects through the androgen receptor (AR) encoded by the Ar gene. Both ERs and AR belong to the nuclear hormone receptor family. They act as ligand-activated transcription modulators by either binding directly to estrogen or androgen responsive elements (EREs or AREs, specific short sequences of DNA), or by associating with other transcription factors [reviewed in [1], [2], [3]]. Both, androgens and estrogens play crucial roles during spermatogenesis. It is well established that testosterone is absolutely essential for maintaining spermatogenesis via the AR present on Sertoli, Leydig and peritubular myoid cells. Since germ cells do not express AR, the androgen-dependent functions of germ cells are thought to be mediated through Sertoli cells [[4], [5], [6]]. Through cell type-specific AR knockout mice models, AR signaling has been shown to be involved in various stages of germ cell development, like meiotic progression, transition from round to elongated spermatids (i.e., spermiogenesis), and sperm release (i.e., spermiation) [reviewed in 7]. Androgens are specifically required for germ cell adhesion to Sertoli cells during spermiogenesis [8], maintenance of the blood-testis barrier [9], and endocytosis during sperm release [10,11]. In the testis, estrogen is produced by Leydig cells, Sertoli cells, and germ cells by the aromatization of testosterone [reviewed in 12]. While both the ERs are present in the germ cells like pachytene and round spermatids, only ERβ is expressed in spermatogonia and Sertoli cells [13,14]. In the adult testis, estrogen is essential for germ cell survival [15,16] and spermiation [17,10]. Estrogen signaling via its two receptors has distinct roles during spermatogenesis; ERα is important during spermiogenesis, while ERβ regulates spermatocyte apoptosis and spermiation [18,10,11].