Hormone Research Center and School of Biological Sciences & Technology, Chonnam National University, Gwangju, Korea.
Endocr J. 2010;57(2):127-34. doi: 10.1507/endocrj.k09e-077. Epub 2009 Nov 19.
The present study examined the gonadotropin regulation of pituitary adenylate cyclase-activating polypeptide (PACAP) and PACAP type I receptor (PAC(1)-R) expression, and its role in progesterone production in the human luteinized granulosa cells. The stimulation of both PACAP and PAC(1)-R mRNA levels by LH was detected using a competitive reverse transcription-polymerase chain reaction (RT-PCR). PACAP transcript was stimulated by LH reaching maximum levels at 12 hours in a dose dependent manner. LH treatment also stimulated PAC(1)-R mRNA levels within 24 hours. Addition of PACAP-38 (10(-7) M) as well as LH significantly stimulated progesterone production during 48 hours culture. Furthermore, co-treatment with PACAP antagonist partially inhibited LH-stimulated progesterone production. Treatment with vasoactive intestinal peptide, however, did not affect progesterone production. Taken together, the present study demonstrates that LH causes a transient stimulation of PACAP and PAC(1)-R expression and that PACAP stimulates progesterone production in the human luteinized granulosa cells, suggesting a possible role of PACAP as a local ovarian regulator in luteinization.
本研究探讨了促性腺激素对垂体腺苷酸环化酶激活肽（PACAP）和 PACAP 型受体（PAC(1)-R）表达的调节作用，以及其在人黄体化颗粒细胞孕激素产生中的作用。采用竞争逆转录聚合酶链反应（RT-PCR）检测 LH 对 PACAP 和 PAC(1)-R mRNA 水平的刺激作用。LH 刺激 PACAP 转录本，呈剂量依赖性，12 小时达到最大水平。LH 处理也在 24 小时内刺激 PAC(1)-R mRNA 水平。在 48 小时培养过程中，添加 PACAP-38（10(-7) M）和 LH 均可显著刺激孕激素的产生。此外，PACAP 拮抗剂的共同处理部分抑制了 LH 刺激的孕激素产生。血管活性肠肽处理并不影响孕激素的产生。综上所述，本研究表明 LH 导致 PACAP 和 PAC(1)-R 表达的短暂刺激，而 PACAP 刺激人黄体化颗粒细胞孕激素的产生，提示 PACAP 可能作为黄体化过程中的局部卵巢调节剂发挥作用。
