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Prolactin Receptor loss with Leydig Cell Apoptosis after EDS treatment of Adult Rats
Author(s) -
Singhal Barkha,
Dutta Dibyendu,
Park In,
Sang Samuel,
Mills Nathaniel
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.575.5
Subject(s) - leydig cell , endocrinology , medicine , sertoli cell , germinal epithelium , receptor , testosterone (patch) , prolactin , biology , interstitial cell , prolactin receptor , testicle , cell , germ cell , spermatogenesis , hormone , gene , luteinizing hormone , biochemistry
Prolactin receptors (Prlr) are reported to be localized to plasma membranes of testicular interstitial cells including Leydig cells. Prlr is also present in Sertoli cell and cells of germinal epithelium (spermatogonia, spermatocytes and elongating spermatids) in the testis. Ethylene dimethane sulfonate (EDS) eliminates Leydig cell in adult rat testes leading to testosterone depletion and germ cell loss. In this study, two Prlr transcript variants (Prl1r & Prl2r) were investigated at times 6, 15, 24 hr, and 5 and 7 days (d) following EDS using RT and qPCR. Rate of Leydig cell loss was evaluated by analysis of insulin‐like peptide 3 mRNA (Insl3), a Leydig cell‐specific marker. Prl2r and Insl3 were less than 1% of normal values in 5 & 7 d EDS‐treated rats. Similar profiles for Prl2r and Insl3 were observed at earlier time points (6, 15 & 24hr). Testosterone replacement after EDS, however, did not restore the levels of Prl2r and Insl3 mRNAs suggesting they are localized to only Leydig cells. In contrast, Prl1r only declined to 40% of normal levels in EDS‐treated rats suggesting that this receptor variant is located in cells of germinal epithelium, as well as Leydig cells. Texas Woman's University‐Research Enhancement Program & Dept. of Biology