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Role of FSH and triiodothyronine in Sertoli cell development expressed by formation of connexin 43-based gap junctions

โœ Scribed by Katarzyna Marchlewska; Krzysztof Kula; Renata Walczak-Jedrzejowska; Elzbieta Oszukowska; Eliza Filipiak; Jolanta Slowikowska-Hilczer


Publisher
Wiley (John Wiley & Sons)
Year
2011
Tongue
English
Weight
265 KB
Volume
315A
Category
Article
ISSN
1932-5223

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โœฆ Synopsis


Abstract

Follicleโ€stimulating hormone (FSH) and triiodothyronine (T3) are known regulatory factors of spermatogenesis initiation. Connexin 43 (Cx43) is the most ubiquitous constitutive protein of gap junctions in the testis. This study evaluates the effects of the hyperstimulation of FSH and T3 during testicular maturation on Cx43 expression in the testis. The newborn, male Wistar rats were divided randomly into four experimental groups: FSH groupโ€”daily injections of FSH 7.5โ€‰IU/animal; T3 groupโ€”100โ€‰ยตg T3/kg body weight; FSH+T3 groupโ€”both substances; A control groupโ€”received vehicles in the same volume. Proliferating cell nuclear antigen immunohistochemistry and toluidine blue staining were used to determine the germ cell proliferation and degeneration. Cx43 immunolocalization was evaluated to find Cx43 maturational changes. Under FSH treatment, the proliferation rate was high so the total number of Sertoli cells increased with a low level of degeneration and lumen formation. T3 stimulation evoked a reduction in the proliferation rate and a decrease in Sertoli cell number but with intensive formation of lumen. T3+FSH inhibited the proliferation rate and stimulated lumen formation together with degeneration, which negatively influenced the number of germ cells in the seminiferous epithelium. We conclude that T3 action seems to be particularly connected with the maturation of Cx43 gap junctions. FSH stimulates maturation of Sertoli cell function, but this effect may take place regardless of the presence of Cx43โ€dependent intercellular communication. The hyperstimulation of both FSH and T3 damages Cx43 connections and hence evokes regressional changes in the seminiferous epithelium. J. Exp. Zool. 315:329โ€“336, 2011. ยฉ 2011 Wileyโ€Liss, Inc.


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