Wilson Kathryn M, Smith A Ian, Phillips David J
Monash Institute of Medical Research, Monash University, Vic. 3800, Australia.
Mol Cell Endocrinol. 2006 Jul 11;253(1-2):30-5. doi: 10.1016/j.mce.2006.03.041. Epub 2006 May 11.
Activin A and its binding protein, follistatin, are released into the circulation following acute systemic inflammation. In this study, we determined the activin and follistatin response of ovine aortic endothelial cells to lipopolysaccharide (LPS). Exposure to LPS for 1h, mimicking a transient inflammatory event, elicited significant increases in activin betaA subunit mRNA or activin A release, with larger, more prolonged increases evident with continuous exposure. On the other hand, follistatin increases were only evident with prolonged exposure to LPS and following increases in activin A release. While cell-associated activin A increased with LPS exposure, levels were lower than those secreted, whereas the opposite was apparent for follistatin. In summary, our findings suggest that vascular endothelial cells, while capable of releasing activin A and follistatin following inflammatory stimulation, are unlikely to be responsible for the rapid release of activin A in vivo following inflammatory challenge.
在急性全身性炎症后，激活素A及其结合蛋白卵泡抑素会释放到循环系统中。在本研究中，我们测定了绵羊主动脉内皮细胞对脂多糖（LPS）的激活素和卵泡抑素反应。暴露于LPS 1小时，模拟短暂的炎症事件，可引起激活素βA亚基mRNA或激活素A释放显著增加，持续暴露时增加幅度更大、持续时间更长。另一方面，卵泡抑素的增加仅在长时间暴露于LPS以及激活素A释放增加后才明显。虽然与细胞相关的激活素A随LPS暴露而增加，但其水平低于分泌水平，而卵泡抑素的情况则相反。总之，我们的研究结果表明，血管内皮细胞虽然能够在炎症刺激后释放激活素A和卵泡抑素，但不太可能是炎症刺激后体内激活素A快速释放的原因。
