Nonsteroidal signals originating in the gonads

Abstract

The discovery of the various peptide factors in the gonads followed different paths. A number of factors were specifically searched for because of physiological experiments that predicted that an activity from the gonads was necessary to explain phenomena. Such was the case for gonadal steroids and for such peptide factors as inhibin, MIS, OMI, FRP, seminal plasma inhibin, relaxin, PA factor and other proteases, and ABP. In the process other factors such as activin and follistatin were serendipitously discovered. A second group of factors was discovered because in vitro experiments of various combinations of gonadal cell types failed to replicate in vivo findings, suggesting missing signals. Such substances are the panoply of growth factors aiding in differentiation and growth promotion and inhibition: LS and LI, P-Mod-S, clusterin, and various components of the ECM. Finally, and most recently, another set of peptides has been identified because immunological or molecular probes have been used to search gonadal tissue for factors originally discovered elsewhere; these include POMC, GnRH-like peptide, oxytocin, AVP, angiotensin, ANF, CRF, neural peptides, and c-mos. Our understanding of the relationship of most of these peptides to the local signals necessary for gonadal function is still very elementary. Clearly some like relaxin and inhibin function as important hormones, and ABP, for example, probably functions importantly in transporting testosterone down the tubule. Most local paracrine or autocrine peptide signals appear to act in relationship to gonadotropin levels probably in local differentiation in the process of gamete maturation, but this is only conjecture at this point. No experimental verification that any of these factors is involved in follicle selection for recruitment or for atresia is yet available. For many of the factors local receptors have not yet been identified. The richness of the variety of peptides in the gonads suggests that microanalysis of cell-cell signaling would be rewarding, but at the time of this writing such investigations are not yet possible.

Beneficial effects of brain-derived neurotropic factor on in vitro maturation of porcine oocytes

“…Although oocyte maturation is triggered by the GTH surge, GTH receptor expression was not detected in either the oocyte itself or its surrounding cumulus cells, but these receptors were expressed in the follicular cells of both theca and granulosa cells (Peng et al 1991). In this context, Ackland et al (1992) previously reported that some paracrine factors, which accumulate in follicular fluid in response to GTH, may affect oocyte maturation. Thus, we propose that these factors could be used in an IVM system, and would be expected to improve its efficiency.…”

Progesterone stimulates pancreatic cell proliferation in vivo

“…However, the present results show that in the progesterone-treated gonadectomized rats high levels of 20a-OHP do not correspond with increased cell proliferation. Next to steroids, the gonads of the male and the female produce and secrete appreciable amounts of all kinds of growth factors, such as activin and inhibin (16,17), members of the transforming growth factor-b superfamily of growth factors, which generally inhibit pancreatic cell replication (18,19), and the insulin-like growth factors-I and -II (20)(21)(22), which are capable of stimulating pancreatic islet-cell proliferation (23). Moreover, in human testis (24) and ovary (25) a growth hormone/placental lactogen variant is produced which also might stimulate cell proliferation in pancreatic tissue (cf.…”

Acute Sex Differences in Serum LH Levels in Gonadectomized Rats: Investigation of Pituitary Response to GnRH Pulse Frequency and Prolactin Secretion as Etiological Agents

“…The rapid rise in serum FSH following gonadectomy in both sexes is due to removal of gonadal inhibin, the major negative regulator of FSH in mammals [25][26][27], Because pituitaries from intact females have been exposed to much higher in vivo inhibin levels than those of males [27], basal FSH release in vitro by pituitaries from intact females is much lower than that of male pituitaries. How ever, in vitro FSH secretion increases with time of basal perifusion by pituitaries from intact females, and is far greater by pituitaries from ovariectomized females, likely due to pituitary withdrawal from high serum inhibin lev els [14], In contrast, exposure to low in vivo levels of serum inhibin by male pituitaries means that male pitu itary FSH experiences less change in relative serum inhi bin levels following gonadectomy, and consequently there is less change in in vitro FSH release by pituitaries from gonadectomized males.…”