Dexamethasone suppresses the differentiation of stem Leydig cells in rats in vitro.


Journal

BMC pharmacology & toxicology
ISSN: 2050-6511
Titre abrégé: BMC Pharmacol Toxicol
Pays: England
ID NLM: 101590449

Informations de publication

Date de publication:
27 05 2019
Historique:
received: 13 10 2018
accepted: 09 05 2019
entrez: 29 5 2019
pubmed: 28 5 2019
medline: 31 1 2020
Statut: epublish

Résumé

It is an established fact that excess of glucocorticoids could cause the harmful effects, such as suppression on the male reproduction. Although glucocorticoids pharmacologically inhibit the Leydig cell function, their roles in Leydig cell development are unclear. Therefore, the present study was designed to investigate effects of synthetic glucocorticoid dexamethasone (DEX) on rat stem Leydig cell proliferation and differentiation. Male Sprague-Dawley rats received a single intraperitoneal injection of 75 mg/kg EDS to eliminate Leydig cells and an in vitro culture system of the seminiferous tubules was established from Leydig cell-depleted testis. Using basal medium and Leydig cell differentiation-inducing medium (LIM) in the culture system, we examined the effects of DEX (0-100 nM) on the proliferation and differentiation of the stem Leydig cells in vitro, respectively. Results showed that LIM is a good agent to induce stem Leydig cell differentiation into Leydig cells that produce testosterone in vitro. DEX inhibited the differentiation of stem Leydig cells by reducing the expression levels of Cyp17a1 and Scarb1 and that NR3C1 antagonist RU38486 reversed the DEX-mediated effects. However, DEX are not involved with the proliferation of stem Leydig cells. DEX suppressed the differentiation of rat Leydig cells in vitro and glucocorticoid-induced effects acted through NR3C1. This suppression partially targets on Cyp17a1 and Scarb1 gene expression.

Sections du résumé

BACKGROUND
It is an established fact that excess of glucocorticoids could cause the harmful effects, such as suppression on the male reproduction. Although glucocorticoids pharmacologically inhibit the Leydig cell function, their roles in Leydig cell development are unclear. Therefore, the present study was designed to investigate effects of synthetic glucocorticoid dexamethasone (DEX) on rat stem Leydig cell proliferation and differentiation.
METHODS
Male Sprague-Dawley rats received a single intraperitoneal injection of 75 mg/kg EDS to eliminate Leydig cells and an in vitro culture system of the seminiferous tubules was established from Leydig cell-depleted testis. Using basal medium and Leydig cell differentiation-inducing medium (LIM) in the culture system, we examined the effects of DEX (0-100 nM) on the proliferation and differentiation of the stem Leydig cells in vitro, respectively.
RESULTS
Results showed that LIM is a good agent to induce stem Leydig cell differentiation into Leydig cells that produce testosterone in vitro. DEX inhibited the differentiation of stem Leydig cells by reducing the expression levels of Cyp17a1 and Scarb1 and that NR3C1 antagonist RU38486 reversed the DEX-mediated effects. However, DEX are not involved with the proliferation of stem Leydig cells.
CONCLUSIONS
DEX suppressed the differentiation of rat Leydig cells in vitro and glucocorticoid-induced effects acted through NR3C1. This suppression partially targets on Cyp17a1 and Scarb1 gene expression.

Identifiants

pubmed: 31133074
doi: 10.1186/s40360-019-0312-z
pii: 10.1186/s40360-019-0312-z
pmc: PMC6537393
doi:

Substances chimiques

Glucocorticoids 0
NR3C1 protein, rat 0
Receptors, Glucocorticoid 0
Scarb1 protein, rat 0
Scavenger Receptors, Class B 0
Dexamethasone 7S5I7G3JQL
CYP17A1 protein, rat EC 1.14.14.19
Steroid 17-alpha-Hydroxylase EC 1.14.14.19

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

32

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Auteurs

Jingwei Zhang (J)

Department of Urology, Shanghai Tenth People's Hospital, Tongji University, Shanghai, China.
Department of Urology, Yijishan Hospital, Wannan Medical College, Wuhu, Anhui, China.

Guanghui Hu (G)

Department of Urology, Shanghai Tenth People's Hospital, Tongji University, Shanghai, China.

Bisheng Huang (B)

Department of Urology, Shanghai Tenth People's Hospital, Tongji University, Shanghai, China.

Dong Zhuo (D)

Department of Urology, Yijishan Hospital, Wannan Medical College, Wuhu, Anhui, China.

Yujie Xu (Y)

Department of Urology, Yijishan Hospital, Wannan Medical College, Wuhu, Anhui, China.

Huitao Li (H)

Center of Scientific Research, the Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China.

Xiangcheng Zhan (X)

Department of Urology, Shanghai Tenth People's Hospital, Nanjing Medical University, Nanjing, Jiangsu, China.

Ren-Shan Ge (RS)

Center of Scientific Research, the Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China. r_ge@yahoo.com.

Yunfei Xu (Y)

Department of Urology, Shanghai Tenth People's Hospital, Tongji University, Shanghai, China. xuyunfeibb@sina.com.

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Classifications MeSH