Fu Li, Osuga Yutaka, Yano Tetsu, Takemura Yuri, Morimoto Chieko, Hirota Yasushi, Schally Andrew V, Taketani Yuji
Department of Obstetrics and Gynecology, Faculty of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, Japan.
Fertil Steril. 2009 Jul;92(1):47-53. doi: 10.1016/j.fertnstert.2008.04.048. Epub 2008 Aug 5.
To determine possible involvement of splice variant 1 (SV1), a variant of the pituitary growth hormone-releasing hormone (GHRH) receptor, in the development of endometriosis.
Comparative and laboratory study.
University teaching hospital reproductive endocrinology and infertility practice.
PATIENT(S): Eutopic and ectopic endometrial tissues, and peritoneal bone marrow-derived cells were collected from women with or without endometriosis. Normal ovarian tissues were collected from women without endometriosis.
INTERVENTION(S): Ectopic endometrial stromal cells (ESC) were isolated and cultured with or without GHRH.
MAIN OUTCOME MEASURE(S): Gene expression of GHRH and SV1 in the sample tissues was determined by reverse transcriptase (RT) nested polymerase chain reaction (PCR). Cyclic adenosine monophosphate (cAMP) production and 5-bromo-2'-deoxyuridine (BrdU) incorporation in ESC were measured using specific assay systems.
RESULT(S): We detected SV1 messenger RNA (mRNA) in 17 out of 27 (63%) ectopic endometrial tissues, which was statistically significantly higher than that detected in eutopic endometrial tissues (2 out of 47, 4%) and normal ovarian tissues (0 out of 14). A relatively low rate of GHRH mRNA was detected in ectopic endometrial tissues (6 out of 27, 24%) and in eutopic endometrial tissues (12 out of 47, 26%). In contrast, relatively high rates were detected in normal ovarian tissues (14 out of 14, 100%) and peritoneal bone marrow-derived cells (13 out of 16, 81%). We found that GHRH stimulated the production of cAMP and the incorporation of BrdU in SV1-expressing ESC.
CONCLUSION(S): GHRH and SV1 may play a role in promoting the development of endometriosis.
确定垂体生长激素释放激素(GHRH)受体的剪接变体1(SV1)是否可能参与子宫内膜异位症的发生发展。
比较性实验室研究。
大学教学医院生殖内分泌与不孕症诊疗科室。
收集有或无子宫内膜异位症女性的在位和异位子宫内膜组织以及腹膜来源的骨髓细胞。收集无子宫内膜异位症女性的正常卵巢组织。
分离异位子宫内膜基质细胞(ESC),并在有或无GHRH的情况下进行培养。
通过逆转录(RT)巢式聚合酶链反应(PCR)测定样本组织中GHRH和SV1的基因表达。使用特定检测系统测量ESC中环状单磷酸腺苷(cAMP)的产生和5-溴-2'-脱氧尿苷(BrdU)的掺入。
我们在27个异位子宫内膜组织中的17个(63%)中检测到SV1信使核糖核酸(mRNA),这在统计学上显著高于在位子宫内膜组织(47个中的2个,4%)和正常卵巢组织(14个中的0个)中检测到的水平。在异位子宫内膜组织(27个中的6个,24%)和在位子宫内膜组织(47个中的12个,26%)中检测到的GHRH mRNA水平相对较低。相比之下,在正常卵巢组织(14个中的14个,100%)和腹膜来源的骨髓细胞(16个中的13个,81%)中检测到相对较高的水平。我们发现GHRH刺激表达SV1的ESC中cAMP的产生和BrdU的掺入。
GHRH和SV1可能在促进子宫内膜异位症的发生发展中起作用。