Adelaide E Weidner, Anna Roy, Kenji Vann, Ariana C Walczyk, Olga Astapova
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引用次数: 0
摘要
Paxillin 是一种普遍表达的适配蛋白,与病灶粘附、细胞运动和细胞凋亡密不可分。最近,Paxillin 还被认为是前列腺癌和其他细胞中雄激素受体(AR)非基因组信号转导的介质。我们试图研究颗粒细胞(GCs)中的 paxillin 与 AR 之间的关系,众所周知,颗粒细胞中的雄激素作用、细胞凋亡和病灶粘附非常重要,但对 paxillin 的作用却研究不足。我们最近的研究表明,敲除小鼠GCs中的paxillin可提高老龄小鼠的生育能力。在这里,我们证明了在人粒细胞衍生的 KGN 细胞中敲除 paxillin 以及在小鼠原生 GCs 中敲除 paxillin 会导致 AR 蛋白表达减少,但不会导致 mRNA 表达减少。此外,我们还发现,在缺乏 paxillin 的情况下,AR 蛋白和 mRNA 的半衰期都会缩短约三分之一,但细胞会通过上调 AR 基因的表达来适应 paxillin 的长期缺失。我们利用共免疫荧光和近接实验表明,paxillin 和 AR 以一种依赖于局灶粘附激酶的方式共定位在 GCs 的质膜上,而局灶粘附的破坏会导致 AR 蛋白水平的降低。我们的研究结果表明,paxillin 将 AR 募集到 GC 膜上,使其免受蛋白酶体降解的影响,并为非基因组信号转导做好准备,这在其他组织中也有报道。为了研究这一点在雄激素过剩疾病中的生理意义,我们在产后长期暴露于二氢睾酮(DHT)诱导的多囊卵巢综合症小鼠模型中测试了GC特异性paxillin基因敲除的效果。对照组小鼠无一例出现发情周期,而33%的paxillin基因敲除小鼠出现了发情周期,这表明paxillin基因缺失可通过减少AR的表达来部分保护小鼠免受雄激素过量的负面影响。与同卵对照组相比,DHT诱导的多囊卵巢综合征小鼠的Paxillin基因敲除GC也能产生更多的雌二醇。因此,paxillin 可能是治疗女性雄激素相关疾病(如多囊卵巢综合症)的一个新靶点。
Paxillin is a ubiquitously expressed adaptor protein integral to focal adhesions, cell motility, and apoptosis. Paxillin has also recently been implicated as a mediator of nongenomic androgen receptor (AR) signaling in prostate cancer and other cells. We sought to investigate the relationship between paxillin and AR in granulosa cells (GCs), where androgen actions, apoptosis, and focal adhesions are of known importance, but where the role of paxillin is understudied. We recently showed that paxillin knockout in mouse GCs increases fertility in older mice. Here, we demonstrate that paxillin knockdown in human granulosa-derived KGN cells, as well as knockout in mouse primary GCs, results in reduced AR protein but not reduced mRNA expression. Further, we find that both AR protein and mRNA half-lives are reduced by approximately one-third in the absence of paxillin, but that cells adapt to chronic loss of paxillin by upregulating AR gene expression. Using co-immunofluorescence and proximity ligation assays, we show that paxillin and AR co-localize at the plasma membrane in GCs in a focal adhesion kinase-dependent way, and that disruption of focal adhesions leads to reduced AR protein level. Our findings suggest that paxillin recruits AR to the GC membrane, where it may be sequestered from proteasomal degradation and poised for nongenomic signaling, as reported in other tissues. To investigate the physiological significance of this in disorders of androgen excess, we tested the effect of GC-specific paxillin knockout in a mouse model of polycystic ovary syndrome (PCOS) induced by chronic postnatal dihydrotestosterone (DHT) exposure. While none of the control mice had estrous cycles, 33% of paxillin knockout mice were cycling, indicating that paxillin deletion may offer partial protection from the negative effects of androgen excess by reducing AR expression. Paxillin-knockout GCs from mice with DHT-induced PCOS also produced more estradiol than GCs from littermate controls. Thus, paxillin may be a novel target in the management of androgen-related disorders in women, such as PCOS.
期刊介绍:
MHR publishes original research reports, commentaries and reviews on topics in the basic science of reproduction, including: reproductive tract physiology and pathology; gonad function and gametogenesis; fertilization; embryo development; implantation; and pregnancy and parturition. Irrespective of the study subject, research papers should have a mechanistic aspect.