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Role of serum- and glucocorticoid-inducible kinase-1 in regulating torsion-induced apoptosis in rats
Serum- and glucocorticoid-inducible kinase-1 (SGK1) is a serine/threonine protein kinase that responds to various stimuli and mediates cell survival. Although it is known that testicular torsion leads to testicular damage and male infertility, the role of SGK1 in torsion remains unclear. This study...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Blackwell Publishing Ltd
2011
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3170482/ https://www.ncbi.nlm.nih.gov/pubmed/20738430 http://dx.doi.org/10.1111/j.1365-2605.2010.01091.x |
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author | Cho, Y-M Pu, H-F Huang, W J Ho, L-T Wang, S-W Wang, P S |
author_facet | Cho, Y-M Pu, H-F Huang, W J Ho, L-T Wang, S-W Wang, P S |
author_sort | Cho, Y-M |
collection | PubMed |
description | Serum- and glucocorticoid-inducible kinase-1 (SGK1) is a serine/threonine protein kinase that responds to various stimuli and mediates cell survival. Although it is known that testicular torsion leads to testicular damage and male infertility, the role of SGK1 in torsion remains unclear. This study investigated whether torsion-induced apoptosis is associated with changes in phosphoinositide-dependent protein kinase-1 (PDK1), SGK1 and forkhead transcription factor FOXO3a expression and/or phosphorylation in rats. Sprague-Dawley rats were divided into four groups: sham (control), 1, 2 and 4 h of unilateral torsion. Bilateral testes, testicular interstitial fluid (TIF) and blood samples were collected immediately after torsion. Our results revealed that SGK1 protein and mRNA were abundantly present in testes and were induced by 2 h of torsion, but that phosphorylation of SGK1, PDK1 and FOXO3a decreased simultaneously. After 2 h of torsion, the testosterone secretion capacity of the primary Leydig cells and testicular interstitial cells (TICs) was impaired and apoptotic spermatogonia and TICs were observed; in addition, the mean seminiferous tubular diameter was decreased. Torsion increased plasma corticosterone levels, but decreased plasma luteinizing hormone and testosterone levels. However, the testosterone levels of the TIF in the ipsilateral testes were significantly enhanced after 2 h of torsion, but suppressed in the contralateral testes. This animal study suggests that PDK1, SGK1 and FOXO3a are involved in torsion-induced apoptosis and that medical therapy should be performed as early as 2 h after the occurrence of torsion to prevent further damage. |
format | Online Article Text |
id | pubmed-3170482 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2011 |
publisher | Blackwell Publishing Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-31704822011-09-14 Role of serum- and glucocorticoid-inducible kinase-1 in regulating torsion-induced apoptosis in rats Cho, Y-M Pu, H-F Huang, W J Ho, L-T Wang, S-W Wang, P S Int J Androl Original Articles Serum- and glucocorticoid-inducible kinase-1 (SGK1) is a serine/threonine protein kinase that responds to various stimuli and mediates cell survival. Although it is known that testicular torsion leads to testicular damage and male infertility, the role of SGK1 in torsion remains unclear. This study investigated whether torsion-induced apoptosis is associated with changes in phosphoinositide-dependent protein kinase-1 (PDK1), SGK1 and forkhead transcription factor FOXO3a expression and/or phosphorylation in rats. Sprague-Dawley rats were divided into four groups: sham (control), 1, 2 and 4 h of unilateral torsion. Bilateral testes, testicular interstitial fluid (TIF) and blood samples were collected immediately after torsion. Our results revealed that SGK1 protein and mRNA were abundantly present in testes and were induced by 2 h of torsion, but that phosphorylation of SGK1, PDK1 and FOXO3a decreased simultaneously. After 2 h of torsion, the testosterone secretion capacity of the primary Leydig cells and testicular interstitial cells (TICs) was impaired and apoptotic spermatogonia and TICs were observed; in addition, the mean seminiferous tubular diameter was decreased. Torsion increased plasma corticosterone levels, but decreased plasma luteinizing hormone and testosterone levels. However, the testosterone levels of the TIF in the ipsilateral testes were significantly enhanced after 2 h of torsion, but suppressed in the contralateral testes. This animal study suggests that PDK1, SGK1 and FOXO3a are involved in torsion-induced apoptosis and that medical therapy should be performed as early as 2 h after the occurrence of torsion to prevent further damage. Blackwell Publishing Ltd 2011-08 /pmc/articles/PMC3170482/ /pubmed/20738430 http://dx.doi.org/10.1111/j.1365-2605.2010.01091.x Text en International Journal of Andrology © 2011 European Academy of Andrology http://creativecommons.org/licenses/by/2.5/ Re-use of this article is permitted in accordance with the Creative Commons Deed, Attribution 2.5, which does not permit commercial exploitation. |
spellingShingle | Original Articles Cho, Y-M Pu, H-F Huang, W J Ho, L-T Wang, S-W Wang, P S Role of serum- and glucocorticoid-inducible kinase-1 in regulating torsion-induced apoptosis in rats |
title | Role of serum- and glucocorticoid-inducible kinase-1 in regulating torsion-induced apoptosis in rats |
title_full | Role of serum- and glucocorticoid-inducible kinase-1 in regulating torsion-induced apoptosis in rats |
title_fullStr | Role of serum- and glucocorticoid-inducible kinase-1 in regulating torsion-induced apoptosis in rats |
title_full_unstemmed | Role of serum- and glucocorticoid-inducible kinase-1 in regulating torsion-induced apoptosis in rats |
title_short | Role of serum- and glucocorticoid-inducible kinase-1 in regulating torsion-induced apoptosis in rats |
title_sort | role of serum- and glucocorticoid-inducible kinase-1 in regulating torsion-induced apoptosis in rats |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3170482/ https://www.ncbi.nlm.nih.gov/pubmed/20738430 http://dx.doi.org/10.1111/j.1365-2605.2010.01091.x |
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