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Int. J. Mol. Sci. 2014, 15(11), 21028-21044; doi:10.3390/ijms151121028

Time-Course Changes of Steroidogenic Gene Expression and Steroidogenesis of Rat Leydig Cells after Acute Immobilization Stress

1
Department of Anesthesiology of the Second Affiliated Hospital
2
Department of Pharmacology of School of Pharmacy, Wenzhou Medical University, Wenzhou 325035, Zhejiang, China
3
Research Academy of Reproductive Biomedicine, Wenzhou Medical University, Wenzhou 325000, Zhejiang, China
4
Huzhou Maternity & Child Care Hospital, Huzhou 313000, Zhejiang, China
These authors contributed equally to this work
*
Authors to whom correspondence should be addressed.
Received: 12 June 2014 / Revised: 26 October 2014 / Accepted: 28 October 2014 / Published: 14 November 2014
(This article belongs to the Section Molecular Toxicology)
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Abstract

Leydig cells secrete testosterone, which is essential for male fertility and reproductive health. Stress increases the secretion of glucocorticoid (corticosterone, CORT; in rats), which decreases circulating testosterone levels in part through a direct action by binding to the glucocorticoid receptors (NR3C1) in Leydig cells. The intratesticular CORT level is dependent on oxidative inactivation of glucocorticoid by 11β-hydroxysteroid dehydrogenase 1 (HSD11B1) in Leydig cells. In the present study, we investigated the time-course changes of steroidogenic gene expression levels after acute immobilization stress in rats. The plasma CORT levels were significantly increased 0.5, 1, 3 and 6 h after immobilization stress, while plasma testosterone levels were significantly reduced 3 and 6 h, after stress and luteinizing hormone (LH) did not change. Immobilization stress caused the down-regulation of Scarb1, Star and Cyp17a1 expression levels in the rat testis starting at the first hour of stress, ahead of the significant decreases of plasma testosterone levels. Other mRNA levels, including Cyp11a1, Hsd3b1 and Hsd17b3, began to decline after 3 h. Hsd11b1 and Nos2 mRNA levels did not change during the course of stress. Administration of glucocorticoid antagonist RU486 significantly restored plasma testosterone levels. In conclusion, Scarb1, Star and Cyp17a1 expression levels are more sensitive to acute stress, and acute immobilization stress causes the decline of the steroidogenic pathway via elevating the levels of glucocorticoid, which binds to NR3C1 in Leydig cells to inhibit steroidogenic gene expression. View Full-Text
Keywords: acute stress; Leydig cell; steroidogenic enzymes; rat; corticosterone; StAR acute stress; Leydig cell; steroidogenic enzymes; rat; corticosterone; StAR
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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Lin, H.; Yuan, K.-M.; Zhou, H.-Y.; Bu, T.; Su, H.; Liu, S.; Zhu, Q.; Wang, Y.; Hu, Y.; Shan, Y.; Lian, Q.-Q.; Wu, X.-Y.; Ge, R.-S. Time-Course Changes of Steroidogenic Gene Expression and Steroidogenesis of Rat Leydig Cells after Acute Immobilization Stress. Int. J. Mol. Sci. 2014, 15, 21028-21044.

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