Cailleau J, Vermeire S, Verhoeven G
Laboratorium voor Experimentele Geneeskunde en Endocrinologie, Department of Developmental Biology, Onderwijs en Navorsing, Gasthuisberg, Leuven, Belgium.
Mol Cell Endocrinol. 1990 Feb 12;69(1):79-89. doi: 10.1016/0303-7207(90)90091-l.
The production of insulin-like growth factor I (IGF-I) and IGF-I binding protein (BP) was investigated in Sertoli, Leydig and peritubular cells derived from the immature rat testis and cultured in vitro. It is demonstrated that all these cells secrete not only IGF-I but also IGF-I BP. In Sertoli cells follitropin (FSH) and other agonists which increase intracellular cAMP stimulate IGF-I secretion but inhibit IGF-I BP release. The response of the BP is pronounced and very sensitive which makes it a new and useful parameter of FSH action. The calcium ionophore A23187 markedly decreases IGF-I BP production in Sertoli cells without noticeable effect on IGF-I itself. This effect can only partially be mimicked by a phorbol ester suggesting that intracellular calcium itself may play a major role in the control of IGF-I BP secretion. Peritubular cells produce high amounts of IGF-I and low amounts of IGF-I BP. Androgens do not affect the production of IGF-I or its BP neither by monocultures nor by cocultures of peritubular and Sertoli cells. In Leydig cells, lutropin (LH) and cAMP stimulate both IGF-I and IGF-I BP secretion. The production of IGF-I by Leydig-Sertoli cocultures clearly exceeds that expected from the monocultures suggesting that cell-cell interactions may also play a role in the control of testicular IGF-I production. The observation that the production of IGF-I and its activity are tightly and independently controlled supports the contention that this growth factor plays an important role in the paracrine and autocrine control of testicular function. Whether IGF-I BP increases or decreases the effects of IGF-I in the testis remains to be investigated.
对源自未成熟大鼠睾丸并在体外培养的支持细胞、间质细胞和管周细胞中胰岛素样生长因子I（IGF-I）及IGF-I结合蛋白（BP）的产生进行了研究。结果表明，所有这些细胞不仅分泌IGF-I，还分泌IGF-I BP。在支持细胞中，促卵泡激素（FSH）和其他增加细胞内cAMP的激动剂刺激IGF-I分泌，但抑制IGF-I BP释放。BP的反应显著且非常敏感，这使其成为FSH作用的一个新的有用参数。钙离子载体A23187显著降低支持细胞中IGF-I BP的产生，而对IGF-I本身无明显影响。佛波酯只能部分模拟这种效应，表明细胞内钙本身可能在IGF-I BP分泌的控制中起主要作用。管周细胞产生大量的IGF-I和少量的IGF-I BP。雄激素无论是通过管周细胞的单培养还是管周细胞与支持细胞的共培养，都不影响IGF-I或其BP的产生。在间质细胞中，促黄体激素（LH）和cAMP刺激IGF-I和IGF-I BP的分泌。间质细胞与支持细胞共培养时IGF-I的产生明显超过单培养预期，这表明细胞间相互作用可能也在睾丸IGF-I产生的控制中发挥作用。IGF-I的产生及其活性受到紧密且独立控制的观察结果支持了这种生长因子在睾丸功能的旁分泌和自分泌控制中起重要作用的观点。IGF-I BP在睾丸中是增强还是减弱IGF-I的作用仍有待研究。
