Mongiat Lucas A, Lux-Lantos Victoria A, Libertun Carlos
Laboratorio de Neuroendocrinología, Instituto de Biología y Medicina Experimental (IBYME), 1428 Buenos Aires, Argentina.
Biol Reprod. 2004 Aug;71(2):464-9. doi: 10.1095/biolreprod.104.027342. Epub 2004 Apr 7.
The participation of type I GnRH receptor (GnRH-R) on GnRH-II-induced gonadotropin secretion in rat pituitary cells was investigated. Furthermore, we extended the study of GnRH-II action to ovarian cells. The GnRH-II was able to mobilize inositol triphosphate (IP(3)) and to induce LH and FSH release in a dose-dependent manner in pituitary cells and in a GnRH-I-like manner. The GnRH-analog 135-18 (agonist for type II GnRH-R and antagonist for type I GnRH-R) was unable to elicit any cellular response tested in these pituitary cells. The GnRH-II responses were blocked by the type I GnRH-R-antagonists CRX or 135-18, suggesting that these effects were mediated by the type I GnRH-R. In contrast to pituitary cells, GnRH-I, but not GnRH-II, elicited an IP(3) response in superovulated ovarian cells; 135-18 also had no effect. However, GnRH-II as well as GnRH-I presented antiproliferative effects on these cells. Surprisingly, 135-18 had stronger antiproliferative effects than either GnRH peptide. The 135-18 analog, but not GnRH-I or GnRH-II, increased progesterone secretion in superovulated ovarian cells. These results strongly suggest that GnRH-II is able to stimulate rat pituitary cells through the type I GnRH-R, with no evidence for the presence of type II GnRH-R. On the other hand, our results indicate a putative GnRH-R in superovulated ovarian cells with response characteristics that differ from those of the GnRH-R in the pituitary.
研究了I型促性腺激素释放激素受体（GnRH-R）在GnRH-II诱导大鼠垂体细胞促性腺激素分泌中的作用。此外，我们将GnRH-II作用的研究扩展到卵巢细胞。GnRH-II能够动员三磷酸肌醇（IP(3)），并以剂量依赖的方式诱导垂体细胞释放促黄体生成素（LH）和促卵泡生成素（FSH），其方式类似于GnRH-I。GnRH类似物135-18（II型GnRH-R激动剂和I型GnRH-R拮抗剂）在这些垂体细胞中未能引发任何测试的细胞反应。GnRH-II反应被I型GnRH-R拮抗剂CRX或135-18阻断，表明这些作用是由I型GnRH-R介导的。与垂体细胞不同，GnRH-I而非GnRH-II在超排卵的卵巢细胞中引发了IP(3)反应；135-18也没有作用。然而，GnRH-II以及GnRH-I对这些细胞具有抗增殖作用。令人惊讶的是，135-18的抗增殖作用比任何一种GnRH肽都更强。135-18类似物而非GnRH-I或GnRH-II增加了超排卵卵巢细胞中的孕酮分泌。这些结果强烈表明，GnRH-II能够通过I型GnRH-R刺激大鼠垂体细胞，没有证据表明存在II型GnRH-R。另一方面，我们的结果表明超排卵卵巢细胞中存在一种假定的GnRH-R，其反应特征与垂体中的GnRH-R不同。
