Leydig cells, which produce the primary male steroid hormone testosterone (T), express the two estrogen receptor (ER) subtypes, ERalpha and ERbeta, and have the capacity to convert testosterone to the natural estrogen 17beta-estradiol. Thus, Leydig cells are subject to estrogen action. The development of transgenic mice that are homozygous for targeted deletion of genes encoding the ER subtypes provides an opportunity to examine the role of estrogen in Leydig cell function. In this study androgen biosynthesis was analyzed in Leydig cells from mice that were homozygous for targeted deletion of the ERalpha gene (alphaERKO). T production by alphaERKO Leydig cells was 2-fold higher than that in wild-type (WT) cells. Serum T levels were accordingly higher in alphaERKO compared with WT mice (5.1 +/- 1.1 vs. 2.2 +/- 0.4 ng/ml; P
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Article Synopsis
- The study investigates adrenomedullin's (ADM) role in protecting estrogen production in Leydig cells by targeting the TGF-β1/Smads signaling pathway.
- Treatment with ADM via recombinant adenovirus (Ad-ADM) in Leydig cells improved cell viability and hormone production in the presence of lipopolysaccharide (LPS), a compound that can induce cellular stress.
- Results indicated that Ad-ADM not only maintained testosterone production and aromatase activity but also reduced the harmful effects of TGF-β1 and Smads, suggesting that ADM supports the overall hormone balance in Leydig cells.
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