Laboratory of Genetics and Exercise Metabolism, Biophysics Department, Federal University of São Paulo (UNIFESP), São Paulo, Brazil.
Molecular Biology Program, Federal University of São Paulo (UNIFESP), São Paulo, Brazil.
Sci Rep. 2021 Jun 1;11(1):11456. doi: 10.1038/s41598-021-90872-6.
Several cytokines have been reported to participate in spermatogenesis, including interleukin-6 (IL6). However, not many studies have been conducted on the loss of Il6 on the male reproductive tract. Nonetheless, there is considerable knowledge regarding the pathological and physiological role of IL6 on spermatogenesis. In this way, this study evaluated the impact of Il6 deficiency on mice testicles in the absence of infection or inflammation. We showed that Il6 deficiency increases daily sperm production, the number of spermatids, and the testicular testosterone and dihydrotestosterone levels. Besides that, mice with a deleted Il6 (IL6KO) showed increased testicular SOCS3 levels, with no changes in pJAK/JAK and pSTAT3/STAT3 ratios. It is worth noting that the aforementioned pathway is not the only pathway to up-regulate SOCS3, nor is it the only SOCS3 target, thus proposing that the increase of SOCS3 in the testis occurs independently of the JAK-STAT signaling in IL6KO mice. Therefore, we suggest that the lack of Il6 drives androgenic production by increasing SOCS3 in the testis, thus leading to an increase in spermatogenesis.
几种细胞因子已被报道参与精子发生，包括白细胞介素-6（IL6）。然而，关于男性生殖道中 Il6 缺失的研究并不多。尽管如此，关于 IL6 对精子发生的病理和生理作用已经有了相当多的认识。在这种情况下，本研究评估了 Il6 缺乏对无感染或炎症的小鼠睾丸的影响。我们发现 Il6 缺乏会增加精子的日产量、精母细胞数量以及睾丸中的睾酮和二氢睾酮水平。此外，缺失 Il6 的小鼠（IL6KO）显示 SOCS3 水平升高，而 pJAK/JAK 和 pSTAT3/STAT3 比值没有变化。值得注意的是，上述途径不是上调 SOCS3 的唯一途径，也不是 SOCS3 的唯一靶标，因此提出 SOCS3 在 IL6KO 小鼠睾丸中的增加独立于 JAK-STAT 信号通路。因此，我们认为缺乏 Il6 通过增加睾丸中的 SOCS3 来驱动雄激素的产生，从而导致精子发生增加。
