Kamanga-Sollo E, White M E, Chung K Y, Johnson B J, Dayton W R
Animal Growth and Development Laboratory, Department of Animal Science, University of Minnesota, 348 ABLMS, Eckles Avenue, St. Paul, MN 55108, USA.
Domest Anim Endocrinol. 2008 Oct;35(3):254-62. doi: 10.1016/j.domaniend.2008.06.001. Epub 2008 Jul 11.
Androgenic and estrogenic steroids enhance muscle growth in animals and humans. Estradiol-17beta (E2) and trenbolone acetate (TBA) (a synthetic testosterone analog) increased IGF-I mRNA expression in bovine muscle satellite cell (BSC) cultures. The goal of this study was to evaluate the mechanisms responsible for this increase by evaluating the effects of ICI 182 780 (an E2 receptor antagonist), flutamide (an androgen receptor inhibitor), G1 (a GPR30 agonist), and BSA-conjugated E2 on E2 and/or TBA-stimulated IGF-I mRNA expression in BSC cultures. Flutamide completely suppressed TBA-stimulated IGF-I mRNA expression in BSC cultures. ICI 182 780 did not suppress E2-stimulated IGF-I mRNA expression and 100 nM ICI 182 780 enhanced (93%, p<0.05) IGF-I mRNA levels in BSC cultures. G1 (100 nM) stimulated IGF-I mRNA expression (100%, p<0.05) but had no effect on proliferation in BSC cultures. E2-BSA, which cannot cross the cell membrane, stimulated IGF-I mRNA expression (approximately 100%, p<0.05) in BSC but even at extremely high concentrations had no effect on proliferation. In summary, our data indicate the E2-stimulation of proliferation and E2-stimulation of IGF-I mRNA expression in BSC cultures occur via different mechanisms. Our previous results showing that ICI 182 780 inhibited BSC proliferation and results of the current study showing lack of response to E2-BSA or G1 suggest that E2-stimulated proliferation in BSC cultures is mediated through classical estrogen receptors. Stimulation by ICI 182 780, G1 and E2-BSA suggests the E2-stimulated IGF-I mRNA expression in BSC cultures is mediated through the GPR30 receptor.
雄激素和雌激素类固醇可促进动物和人类的肌肉生长。17β-雌二醇（E2）和醋酸群勃龙（TBA，一种合成睾酮类似物）可增加牛肌肉卫星细胞（BSC）培养物中IGF-I mRNA的表达。本研究的目的是通过评估ICI 182 780（一种E2受体拮抗剂）、氟他胺（一种雄激素受体抑制剂）、G1（一种GPR30激动剂）和牛血清白蛋白偶联E2（E2-BSA）对BSC培养物中E2和/或TBA刺激的IGF-I mRNA表达的影响，来评估导致这种增加的机制。氟他胺完全抑制了BSC培养物中TBA刺激的IGF-I mRNA表达。ICI 182 780没有抑制E2刺激的IGF-I mRNA表达，100 nM的ICI 182 780可提高（93%，p<0.05）BSC培养物中IGF-I mRNA水平。G1（100 nM）刺激了IGF-I mRNA表达（100%，p<0.05），但对BSC培养物的增殖没有影响。不能穿过细胞膜的E2-BSA刺激了BSC中IGF-I mRNA表达（约100%，p<0.05），但即使在极高浓度下对增殖也没有影响。总之，我们的数据表明，BSC培养物中E2对增殖的刺激和E2对IGF-I mRNA表达的刺激是通过不同机制发生的。我们之前的结果表明ICI 182 780抑制了BSC增殖，而本研究结果表明对E2-BSA或G1无反应，这表明BSC培养物中E2刺激的增殖是通过经典雌激素受体介导的。ICI 182 780、G1和E2-BSA的刺激表明，BSC培养物中E2刺激的IGF-I mRNA表达是通过GPR30受体介导的。
