This growth factor, in fact, has been demonstrated to act also as a survival factor for male germ cells since it is capable to significantly decrease germ cell apoptosis Leydig cells As well as mouse fetal Leydig cells, also Leydig cells isolated from pubertal rats expressed c-Met receptor Several growth factors have been described as local modulators of Sertoli cell physiological niche and HGF can be numbered in this cohort since it has been demonstrated as a paracrine and autocrine modulator of Sertoli cell physiology. All together these data indicate that HGF has a role in the control of spermatogenesis and sperm quality either directly, acting on male germ cells, or indirectly acting on tubular and interstitial somatic cells of the testis. It is well known that germ cell proliferation and survival are controlled by endocrine signals:
BTB separates the seminiferous epithelium in two different niches: In addition, HGF modifies the position of the tight junctions: Moreover, it has been reported that HGF may induce mesenchymal to epithelial cell conversion Thus HGF acts as a paracrine factor even on differentiating fetal Leydig cells reproducing in the interstitial compartment the epithelium—mesenchyme cross-talk present between interstitium and testicular cords in the embryonic stages before this pre-natal age. This result on spermatogonia cells appears to be more relevant highlighting that the HGF activator inhibitor HAI-2 is expressed exclusively in primary spermatocytes 69 strongly indicating that mitotic germ cells need HGF signal whereas at the beginning of meiotic process this proliferating cue needs to be inhibited in order to allow germ cell meiotic entry. What seems noteworthy is that the distribution patterns and functional roles of this molecular machinery change in the different morphogenetic phases of the testicular embryonic development. A hematoxylin—eosin stained section of rodent adult testis is also reported. Alternatively, this observation could be due to the presence of a more complex network of pro-apoptotic and anti-apoptotic factors present in the older animals Figure 2. It is fair to highlight the parallelism between male and female gonad and to notice that steroid production modulation in response to local cues is quite relevant for gonad physiology since sex hormones are not only important for endocrine homeostasis via pituitary—gonadal axis cross-talk but also act as paracrine regulators of male and female gametogenesis. This system, in fact, has been found in several developing organs being HGF expressed in the mesenchyme and c-Met in the epithelial part of the developing tissue. The activities of the HGF machinery on the testicular tissue vary depending on the different phases of both pre-natal and post-natal ages: This review has the aim to summarize what is currently known regarding this topic. Noteworthy changes in HGF concentration in seminal plasma have been reported in different andrological diseases. It was suggested that modifications in HGF seminal plasma concentration could be related with different andrological diseases and male infertility, but actually as in this case conflicting data are reported in the literature 87 — Besides its action as a hormone, it has been demonstrated that HGF expression is regulated by blood hormones, neurotransmitters, and cytokines, such as GH 26 , Norepinephrine 27 , and systemic prostaglandin E Despite this observation, in the post-natal testis, HGF has often been demonstrated to be expressed also by the same cell lineages that express c-Met and Sertoli cells are not an exception. HGF administration on isolated Leydig cells significantly reduces the amount of fibronectin indicating that this growth factor might modify interstitial extracellular matrix components and in turn changes significantly adhesive microenvironment and cytokine availability Figure 2. As HGF has been proposed as one of the factors able to modify Sertoli cell physiology and to maintain their differentiated phenotype, it is conceivable to hypothesize that this factor has a role in the modulation of gonad—pituitary cross-talk. Intriguingly, the steroid modulator activity is not confined in male gonad but was also described in theca cells, which are the Leydig cell ovarian counterparts. In particular, c-Met activation by its ligand HGF triggers transphosphorylation of the catalytic tyrosines Tyr and Tyr , which positively modulate its enzymatic activity. There has not been a report of any effect of HGF on meiotic germ cells, even if they express c-Met receptor on their surface In rat theca cells, in fact, HGF suppressed LH-dependent androsterone secretion, while stimulated basal and LH-induced progesterone production It is fair to highlight that extracellular matrix homeostasis is necessary for spermatogenesis and that a thickened lamina propria has been reported associated with impaired spermatogenesis and that HGF has demonstrated to have anti-fibrotic effect in the regulation of extracellular matrix composition even in other organs 8. The first finding that strongly suggested a role of HGF in epididymal sperm maturation was reported by Naz and coworkers in It is fair to notice that male infertility could be due to really different causes: Picture summarizing the main effects exerted by HGF during embryonic testis development.
Video about hgf sex:
Nasa Mala Klinika- Sestra Mira (upskirt)
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