Testosterone regulates granzyme K expression in rat testes
Objective. Testosterone depletion induces increased germ cell apoptosis in testes. However, limited studies exist on genes that regulate the germ cell apoptosis. Granzymes (GZM) are serine proteases that induce apoptosis in various tissues. Multiple granzymes, including GZMA, GZMB and GZMN, are pres...
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oai:doaj.org-article:cd61b658639f4044b21c620afe217f1c2021-12-02T19:10:31ZTestosterone regulates granzyme K expression in rat testes1336-032910.1515/enr-2017-0020https://doaj.org/article/cd61b658639f4044b21c620afe217f1c2017-10-01T00:00:00Zhttps://doi.org/10.1515/enr-2017-0020https://doaj.org/toc/1336-0329Objective. Testosterone depletion induces increased germ cell apoptosis in testes. However, limited studies exist on genes that regulate the germ cell apoptosis. Granzymes (GZM) are serine proteases that induce apoptosis in various tissues. Multiple granzymes, including GZMA, GZMB and GZMN, are present in testes. Th us, we investigated which granzyme may be testosterone responsive and possibly may have a role in germ cell apoptosis aft er testosterone depletion. Methods. Ethylene dimethane sulfonate (EDS), a toxicant that selectively ablates the Leydig cells, was injected into rats to withdraw the testosterone. The testosterone depletion effects after 7 days post-EDS were verified by replacing the testosterone exogenously into EDS-treated rats. Serum or testicular testosterone was measured by radioimmunoassay. Using qPCR, mRNAs of granzyme variants in testes were quantified. The germ cell apoptosis was identified by TUNEL assay and the localization of GZMK was by immunohistochemistry. Results. EDS treatment eliminated the Leydig cells and depleted serum and testicular testosterone. At 7 days post-EDS, testis weights were reduced 18% with increased germ cell apoptosis plus elevation GZMK expression. GZMK was not associated with TUNEL-positive cells, but was localized to stripped cytoplasm of spermatids. In addition, apoptotic round spermatids were observed in the caput epididymis. Conclusions. GZMK expression in testes is testosterone dependent. GZMK is located adjacent to germ cells in seminiferous tubules and the presence of apoptotic round spermatids in the epididymis suggest its role in the degradation of microtubules in ectoplasmic specializations. Thus, overexpression of GZMK may indirectly regulate germ cell apoptosis by premature release of round spermatids from seminiferous tubule lumen.Dutta DibyenduPark InGuililat HiwotSang SamuelTalapatra ArpitaSinghal BarkhaMills Nathaniel C.Sciendoarticleapoptosisethylene dimethane sulfonateepididymisblood-testis barrierround spermatidstransition protein 1Diseases of the endocrine glands. Clinical endocrinologyRC648-665ENEndocrine Regulations, Vol 51, Iss 4, Pp 193-204 (2017) |
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apoptosis ethylene dimethane sulfonate epididymis blood-testis barrier round spermatids transition protein 1 Diseases of the endocrine glands. Clinical endocrinology RC648-665 |
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apoptosis ethylene dimethane sulfonate epididymis blood-testis barrier round spermatids transition protein 1 Diseases of the endocrine glands. Clinical endocrinology RC648-665 Dutta Dibyendu Park In Guililat Hiwot Sang Samuel Talapatra Arpita Singhal Barkha Mills Nathaniel C. Testosterone regulates granzyme K expression in rat testes |
description |
Objective. Testosterone depletion induces increased germ cell apoptosis in testes. However, limited studies exist on genes that regulate the germ cell apoptosis. Granzymes (GZM) are serine proteases that induce apoptosis in various tissues. Multiple granzymes, including GZMA, GZMB and GZMN, are present in testes. Th us, we investigated which granzyme may be testosterone responsive and possibly may have a role in germ cell apoptosis aft er testosterone depletion. Methods. Ethylene dimethane sulfonate (EDS), a toxicant that selectively ablates the Leydig cells, was injected into rats to withdraw the testosterone. The testosterone depletion effects after 7 days post-EDS were verified by replacing the testosterone exogenously into EDS-treated rats. Serum or testicular testosterone was measured by radioimmunoassay. Using qPCR, mRNAs of granzyme variants in testes were quantified. The germ cell apoptosis was identified by TUNEL assay and the localization of GZMK was by immunohistochemistry. Results. EDS treatment eliminated the Leydig cells and depleted serum and testicular testosterone. At 7 days post-EDS, testis weights were reduced 18% with increased germ cell apoptosis plus elevation GZMK expression. GZMK was not associated with TUNEL-positive cells, but was localized to stripped cytoplasm of spermatids. In addition, apoptotic round spermatids were observed in the caput epididymis. Conclusions. GZMK expression in testes is testosterone dependent. GZMK is located adjacent to germ cells in seminiferous tubules and the presence of apoptotic round spermatids in the epididymis suggest its role in the degradation of microtubules in ectoplasmic specializations. Thus, overexpression of GZMK may indirectly regulate germ cell apoptosis by premature release of round spermatids from seminiferous tubule lumen. |
format |
article |
author |
Dutta Dibyendu Park In Guililat Hiwot Sang Samuel Talapatra Arpita Singhal Barkha Mills Nathaniel C. |
author_facet |
Dutta Dibyendu Park In Guililat Hiwot Sang Samuel Talapatra Arpita Singhal Barkha Mills Nathaniel C. |
author_sort |
Dutta Dibyendu |
title |
Testosterone regulates granzyme K expression in rat testes |
title_short |
Testosterone regulates granzyme K expression in rat testes |
title_full |
Testosterone regulates granzyme K expression in rat testes |
title_fullStr |
Testosterone regulates granzyme K expression in rat testes |
title_full_unstemmed |
Testosterone regulates granzyme K expression in rat testes |
title_sort |
testosterone regulates granzyme k expression in rat testes |
publisher |
Sciendo |
publishDate |
2017 |
url |
https://doaj.org/article/cd61b658639f4044b21c620afe217f1c |
work_keys_str_mv |
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_version_ |
1718377117077471232 |