Effects of the transmethylation inhibitor S-adenosyl-homocysteine and of the methyl donor S-adenosyl-methionine on rat leydig cell function In vitro

1987 ◽  
Vol 26 (1) ◽  
pp. 93-98 ◽  
Author(s):  
V. Papadopoulos ◽  
P. Kamtchouing ◽  
M.A. Drosdowsky ◽  
S. Carreau
1985 ◽  
Vol 132 (2) ◽  
pp. 729-734 ◽  
Author(s):  
M. Benahmed ◽  
C. Grenot ◽  
E. Tabone ◽  
P. Sanchez ◽  
A.M. Morera

1995 ◽  
Vol 134 (1) ◽  
pp. 18-25 ◽  
Author(s):  
L.B. Biegel ◽  
R.C.M. Liu ◽  
M.E. Hurtt ◽  
J.C. Cook

2018 ◽  
Vol 374 (2) ◽  
pp. 389-412 ◽  
Author(s):  
M. Kotula-Balak ◽  
P. Pawlicki ◽  
A. Milon ◽  
W. Tworzydlo ◽  
M. Sekula ◽  
...  

1984 ◽  
Vol 438 (1 Hormonal Cont) ◽  
pp. 684-687 ◽  
Author(s):  
M. BENAHMED ◽  
J. REVENTOS ◽  
E. TABONE ◽  
J. M. SAEZ

Endocrinology ◽  
2021 ◽  
Author(s):  
Pierre-Olivier Hébert-Mercier ◽  
Francis Bergeron ◽  
Nicholas M Robert ◽  
Samir Mehanovic ◽  
Kenley Joule Pierre ◽  
...  

Abstract Leydig cells produce androgens that are essential for male sex differentiation and reproductive function. Leydig cell function is regulated by several hormones and signaling molecules, including growth hormone (GH). Although GH is known to upregulate Star gene expression in Leydig cells, its molecular mechanism of action remains unknown. The STAT5B transcription factor is a downstream effector of GH signaling in other systems. While STAT5B is present in both primary and Leydig cell lines, its function in these cells has yet to be ascertained. Here we report that treatment of MA-10 Leydig cells with GH or overexpression of STAT5B induces Star mRNA levels and increases steroid hormone output. The mouse Star promoter contains a consensus STAT5B element (TTCnnnGAA) at -756 bp to which STAT5B binds in vitro (EMSA and supershift) and in vivo (ChIP) in a GH-induced manner. In functional promoter assays, STAT5B was found to activate a -980 bp mouse Star reporter. Mutating the -756 bp element prevented STAT5B binding but did not abrogate STAT5B-responsiveness. STAT5B was found to functionally cooperate with DNA-bound cJUN. The STAT5B/cJUN cooperation was only observed in Leydig cells and not in Sertoli or fibroblast cells, indicating that additional Leydig cell-enriched transcription factors are required. The STAT5B/cJUN cooperation was lost only when both STAT5B and cJUN elements were mutated. In addition to identifying the Star gene as a novel target for STAT5B in Leydig cells, our data provide important new insights into the mechanism of GH and STAT5B action in the regulation of Leydig cell function.


2013 ◽  
Vol 33 (10) ◽  
pp. 1017-1039 ◽  
Author(s):  
Pallav Sengupta ◽  
Rajdeb Banerjee

This review comprehensively summarizes the effects of more than 15 mostly used pesticides on male reproductive physiology, as recent experimental and epidemiological research have indicated their alarming impact on overall human health. Mechanisms have described that pesticide exposure damages spermatozoa, alter Sertoli or Leydig cell function, both in vitro and in vivo and thus affects semen quality. But, the literature suggests a need for more intricate research in those pesticides that are defined as mutagens or carcinogens and directly affect the hypothalamic–pituitary–gonadal axis. This literature review also proposes specific solutions to overcome these health effects.


Metabolism ◽  
1994 ◽  
Vol 43 (5) ◽  
pp. 533-537 ◽  
Author(s):  
Joseph Tai ◽  
Wah Jun Tze ◽  
Noriko Murase ◽  
Thomas E. Starzl

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