Department of Biochemistry and Molecular Biology, Nankai University School of Medicine, Tianjin, People's Republic of China.
College of Pharmacy, Nankai University, Tianjin, People's Republic of China.
Fertil Steril. 2013 Jan;99(1):256-263.e3. doi: 10.1016/j.fertnstert.2012.09.011. Epub 2012 Oct 6.
To determine differential expression of G-protein-coupled receptor 30 (GPR30) in uterine leiomyoma and its matched myometrium.
GPR30 expression examined in both tissues and cultured cells.
Research laboratories.
PATIENT(S): Women 35 to 50 years old with uterine leiomyomas.
INTERVENTION(S): Hysterectomy.
MAIN OUTCOME MEASURE(S): GPR30 expression profile.
RESULT(S): Using Western blot and real-time quantitative polymerase chain reaction analyses, we found that GPR30 was highly expressed in uterine leiomyomas compared with their matched myometrium. In only three out of nine patients examined was GPR30 protein detectable by Western blot analysis in myometrial tissues, but at statistically significantly lower levels than in their leiomyomas. Confocal microscopy revealed the nuclear localization of GPR30 in leiomyoma tissues and cultured leiomyoma smooth muscle cells (SMCs). Treatment with 0.1 μM 17β-estradiol increased mRNA expression of GPR30 in leiomyoma SMCs but decreased expression in myometrial SMCs. Treatment with G-1, a GPR30 agonist, stimulated phosphorylation of p44/42 mitogen-activated protein kinase (MAPK) in both SMC types. PD98059, the MEK inhibitor, completely inhibited G-1-induced phosphorylation of p44/42 in myometrium SMCs, but not in SMCs from leiomyoma.
CONCLUSION(S): GPR30 is abundantly expressed in uterine leiomyomas, likely resulting from estrogen stimulation.
确定 G 蛋白偶联受体 30（GPR30）在子宫肌瘤及其配对的子宫肌层中的差异表达。
在组织和培养细胞中检查 GPR30 表达。
研究实验室。
年龄 35 至 50 岁的患有子宫肌瘤的女性。
子宫切除术。
GPR30 表达谱。
通过 Western blot 和实时定量聚合酶链反应分析，我们发现 GPR30 在子宫肌瘤中的表达明显高于其配对的子宫肌层。在九名患者中，仅三名患者的子宫肌层组织中可通过 Western blot 分析检测到 GPR30 蛋白，但统计学上明显低于子宫肌瘤。共聚焦显微镜显示 GPR30 在子宫肌瘤组织和培养的子宫肌瘤平滑肌细胞（SMC）中的核定位。用 0.1 μM 17β-雌二醇处理可增加子宫肌瘤 SMC 中 GPR30 的 mRNA 表达，但降低了子宫肌层 SMC 中的表达。GPR30 激动剂 G-1 处理可刺激两种 SMC 类型中 p44/42 丝裂原激活蛋白激酶（MAPK）的磷酸化。MEK 抑制剂 PD98059 完全抑制了 G-1 在子宫肌层 SMC 中诱导的 p44/42 的磷酸化，但对子宫肌瘤 SMC 没有抑制作用。
GPR30 在子宫肌瘤中大量表达，可能是由雌激素刺激所致。
