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首页> 外文期刊>Journal of cellular physiology. >Androgen-dependent miR-125a-5p targets LYPLA1 and regulates global protein palmitoylation level in late-onset hypogonadism males
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Androgen-dependent miR-125a-5p targets LYPLA1 and regulates global protein palmitoylation level in late-onset hypogonadism males

机译：Androgen-dependent mir - 125 - 5 - p LYPLA1和目标调节全球蛋白质棕榈酰化水平晚发性男性性腺机能减退

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摘要

Late-onset hypogonadism (LOH) is defined as a clinical and biochemical syndrome with multiple symptoms caused by testosterone deficiency in aging males. An in-depth exploration of the molecular mechanism underlying LOH development is insufficient. We previously identified miR-125a-5p as a dysregulated microRNA in LOH patients and potential diagnostic biomarker for LOH. The present study demonstrated that plasma miR-125a-5p was upregulated after testosterone supplementation in both LOH patients and castrated mice, and positively associated with the testosterone concentrations, suggesting direct regulation of miR-125a-5p expression by testosterone. Androgen response element in the promoter of miR-125a-5p was subsequently identified. Target gene screening and confirmation verified that LYPLA1, encoding acyl-protein thioesterase 1 which catalyzed protein depalmitoylation process, was a target gene of miR-125a-5p. Furthermore, in cells cultured with testosterone deprivation and organs from castrated mice, testosterone deficiency led to decreased global protein palmitoylation level. In aging males, global protein palmitoylation in peripheral blood showed a notable decline in LOH patients contrast to the normal elderly males. And the palmitoylation level was positively correlative with serum testosterone concentrations. Our results suggested that testosterone could regulate global palmitoylation level through miR-125a-5p/LVPLAl signaling pathway. Given that protein palmitoylation is pivotal for protein function and constitutes the pathogenesis of various diseases, testosterone/miR-125a-5p/LVPLAl may contribute to the molecular mechanism underlying multiple symptoms caused by testosterone deficiency in LOH patients, and aberrant global palmitoylation could be a potential biomarker for LOH.
机译：迟发性性功能减退(LOH)被定义为一个临床和生化综合症与多个睾丸素不足引起的症状老年男性。底层LOH发展分子机制不够的。mir - 125 a - 5 - p作为microRNA在LOH特异表达病人和潜在的诊断生物标记LOH。mir - 125 a - 5 - p在睾丸激素调节在LOH病人和补充被阉割的老鼠,并积极联系在一起睾酮浓度,建议直接的监管mir - 125 - 5 - p的表达睾丸激素。促进mir - 125 a - 5 - p随后识别。确认验证,LYPLA1编码acyl-protein thioesterase 1催化蛋白质depalmitoylation过程,是一个目标基因mir - 125 - 5 - p。培养与睾酮不足和器官从去势小鼠睾丸素不足导致减少全球蛋白质棕榈酰化水平。在衰老的雄性,全球蛋白质棕榈酰化外周血LOH显示显著的下降患者与正常的老年男性。和正十六烷酰化水平相关与血清睾酮浓度。睾酮可能调节全球棕榈酰化水平通过mir - 125 - 5 - p / LVPLAl信号途径。关键蛋白质功能和构成各种疾病的发病机制,睾酮/ mir - 125 - a - 5 - p / LVPLAl可能导致多个背后的分子机制症状在LOH睾丸素不足造成的病人,和全球棕榈酰化异常可能是LOH的潜在生物标志物。

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