Comparative expression and localization of visfatin, chemerin, and chemerin receptor proteins in a heat-stressed mouse testis

被引:2
作者
Jerang, Miti [1 ]
Kumar, Rahul [2 ]
Gurusubramanian, Guruswami [1 ]
Roy, Vikas Kumar [1 ]
机构
[1] Mizoram Univ, Dept Zool, Aizawl 796004, Mizoram, India
[2] Mahatma Gandhi Cent Univ, Dept Biotechnol, Motihari 845401, Bihar, India
关键词
Testis; Heat; -stress; Visfatin; Chemerin; Chemerin receptor; GERM-CELL DEATH; GENE-EXPRESSION; SERTOLI CELLS; RAT TESTIS; ADIPOKINES; APOPTOSIS; TESTOSTERONE; INDUCTION; CRYPTORCHIDISM; HYPERTHERMIA;
D O I
10.1016/j.tice.2024.102374
中图分类号
R602 [外科病理学、解剖学]; R32 [人体形态学];
学科分类号
100101 ;
摘要
The adipokines, visfatin, chemerin, and its receptor are expressed in the testis. It has also been shown that heatstress alters the secretion and expression of other adipokines. Testicular heat-stress is now well known to cause the impairment in the testis. It has also been documented that heat-stress changes the expression of genes and proteins in the testis. To the best of our knowledge, the expression and localization of visfatin chemerin and its receptor have not been investigated in the heat-stressed testis. Therefore, the present study has investigated the expression and localization of these proteins in the heat-stressed testis. The expression of visfatin and chemerin and receptor exhibits a differential repossess against the heat stress. Visfatin expression was up-regulated while chemerin and chemerin receptor was down-regulated in the heat-stressed testis as shown by western blot analysis. The immunolocalization of visfatin and chemerin showed increased abundance in the seminiferous tubules of heat-stressed mice testis. Furthermore, abundance of visfatin, chemerin, and its receptor showed a decrease in abundance in the Leydig cells of heat-stressed testis. The decreased abundance of these proteins in the Leydig cells coincides with decreased 3 beta-HSD immunostaining along with decreased testosterone levels. These results suggest that heat-stress might decrease testosterone secretion by modulating visfatin and chemerin in the Leydig cells. The increased abundance of visfatin and chemerin in the primary spermatocytes, round spermatid, and multinucleated germ cells also coincides with increased immunostaining of active caspase-3. Moreover, expression of Bcl-2 was down-regulated, and expression of active caspase-3 and HSP70 were up-regulated along with increased oxidative stress in the heat-stressed testis, suggesting stimulated apoptosis. In conclusion, our results showed that visfatin, chemerin, and its receptor are differentially expressed in the testis under heat-stress and within the testis also it might differentially regulate testosterone biosynthesis in the Leydig cells and apoptosis in the seminiferous tubules.
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页数:12
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