Calcium confusion--is the variability in calcium response by Sertoli cells to specific hormones meaningful or simply redundant?

Abstract

When results of more than ten different studies on hormone-induced calcium signals in Sertoli cells are taken together, a wide variety of responses emerges. The reported changes range from increased concentrations, via no response at all, to decreased calcium concentrations. Minor variations in cell isolation techniques, culture conditions, or techniques for measuring the intracellular calcium could explain some of these differences. However, erratic variations in response are also observed within research groups under very similar experimental conditions. Such 'negative' findings are mainly reported orally and do not further penetrate the scientific community. As hormone-dependent calcium responses evidently may depend very much on the context of the cells, calcium transients would appear to be unreliable bioassay principles with which to detect the primary actions of FSH and effectors such as androgens on Sertoli cells. A more important biological question is whether these sometimes opposed calcium transients are connected with a particular cellular response. To date there is no evidence for such a tight coupling in Sertoli cells, implying that, at least under in vitro conditions, calcium signals might even be redundant altogether. Such calcium variability is probably not unique to Sertoli cells, and the aim of this commentary is to promote an open debate that may help to transform the current state of 'calcium confusion' into a better understanding of the intracellular calcium language.

Diverse FSH and Testosterone Signaling Pathways in the Sertoli Cell

“…Possible explanations for these differences include: the diverse [Ca 2 + ]i compartmentalization; differences in cross talk on the postreceptor signaling pathways; and differences in the amplitude and / or frequency of the Ca 2 + oscillations. Also, hormonedependent calcium responses may depend very much on the functional context of the cell [49] .…”

Inhibitory actions of mibefradil on steroidogenesis in mouse Leydig cells: involvement of Ca2+ entry via the T-type Ca2+ channel

“…Ca 2+ helps regulate a variety of cellular functions in many different cells, including germ cells and somatic cells in the testis, as well as spermatozoa, in response to endocrine hormones and local regulators [7][8][9][10][11]. Moreover, alteration of the Ca 2+ signalling pathway has a drastic impact on many cellular physiologies [12][13][14][15] [5,6,17], while other studies have argued that voltage-dependent Ca 2+ channels (VDCCs) are also involved [18][19][20].…”

Effects of L- and T-type Ca2+ channel blockers on spermatogenesis and steroidogenesis in the prepubertal mouse testis

“…For instance, FSH and LH exerts their actions on steroidogenesis by mainly regulating intracellular Ca 2+ concentration through VDCCs in Sertoli cells [27,28] and Leydig cells [29]. Thus, it is possible, and even likely, that any malfunction of Ca 2+ channels in somatic cells may result in a drastic attenuation or a complete failure of spermatogenesis and steroidogenesis.…”