Weber G M, Sullivan C V
Department of Zoology, North Carolina State University, Campus Box 7617, Raleigh, NC 27695-7617, USA.
Comp Biochem Physiol B Biochem Mol Biol. 2001 Jun;129(2-3):467-73. doi: 10.1016/s1096-4959(01)00349-9.
Oocyte germinal vesicle breakdown (GVBD) was induced in striped bass ovarian fragments when tissues were incubated with 100-nM recombinant human insulin-like growth factor-I (rhIGF-I), 25-IU human chorionic gonadotropin (hCG) ml(-1), or 290 nM of the maturation-inducing steroid (MIS), 17,20beta,21-trihydroxy-4-pregnen-3-one (20beta-S). Inhibitors of phosphatidylinositol 3-kinase (PI 3-K), wortmannin (100 nM) and LY 294002 (50 microM), inhibited GVBD induced by these hormones. Furthermore, the inhibitors attenuated hCG-induced steroid hormone synthesis. Previous studies report that gap junction uncouplers inhibit GVBD induced by hCG, but not by rhIGF-I, in striped bass. We show that 20beta-S-induced GVBD is also attenuated by 1 mM 1-heptanol or 1-octanol without being affected by incubation with 3 mM ethanol. Thus, the effects of inhibiting PI 3-K activity on GtH and MIS actions are similar to effects of uncoupling gap junctions. These data suggest that PI 3-K activity is required for GtH- MIS- and IGF-I induction of GVBD in striped bass. Our data are also consistent with the notion that a ligand that regulates PI 3-K activity, possibly an IGF, participates in maintenance of gap junctional communication required for maximal GtH and MIS action.
当条纹鲈卵巢组织片段与100 nM重组人胰岛素样生长因子-I（rhIGF-I）、25 IU人绒毛膜促性腺激素（hCG）/ml或290 nM成熟诱导类固醇（MIS）17,20β,21-三羟基-4-孕烯-3-酮（20β-S）一起孵育时，卵母细胞生发泡破裂（GVBD）被诱导。磷脂酰肌醇3-激酶（PI 3-K）抑制剂渥曼青霉素（100 nM）和LY 294002（50 μM）抑制了这些激素诱导的GVBD。此外，这些抑制剂减弱了hCG诱导的类固醇激素合成。先前的研究报道，间隙连接解偶联剂抑制条纹鲈中hCG诱导的GVBD，但不抑制rhIGF-I诱导的GVBD。我们发现，20β-S诱导的GVBD也会被1 mM 1-庚醇或1-辛醇减弱，而与3 mM乙醇孵育则不会产生影响。因此，抑制PI 3-K活性对促性腺激素（GtH）和MIS作用的影响与间隙连接解偶联的影响相似。这些数据表明，条纹鲈中GtH、MIS和IGF-I诱导GVBD需要PI 3-K活性。我们的数据还与以下观点一致：一种调节PI 3-K活性的配体，可能是一种IGF，参与维持最大GtH和MIS作用所需的间隙连接通讯。
