Ohga E, Matsuse T, Teramoto S, Ouchi Y
Department of Geriatric Medicine, University of Tokyo, Japan.
Life Sci. 2000 Mar;66(17):1603-13. doi: 10.1016/s0024-3205(00)00480-x.
Activin A is a member of the transforming growth factor-beta superfamily that exerts its diverse biological effects through bindings to activin specific transmembrane serine/threonine kinase receptors. The fibroblast-mediated contraction of a collagen gel is thought to be a model of part of the wound-repair response and tissue contraction. In this study, we found the expression of activin type I receptors (ActR-I and ActR-IB) and type II receptor (ActR-II) on human fetal lung fibroblasts (HFL-1) by RT-PCR and immunocytochemistry. We also examined the effects of activin A on the HFL-1-mediated collagen gel contraction. Activin A stimulated collagen gel contraction in a dose dependent manner and its effect was abolished by an activin-binding protein, follistatin, that specifically suppresses activin A activities. This study demonstrated that ActR-I, ActR-1B and ActR-II are expressed on human fetal lung fibroblast and that activin A regulates fibroblast-mediated collagen gel contraction, suggesting that activin A might contribute to human lung fibroblast activities and structural remodeling observed in pulmonary fibrosis.
激活素A是转化生长因子-β超家族的成员，它通过与激活素特异性跨膜丝氨酸/苏氨酸激酶受体结合发挥多种生物学效应。成纤维细胞介导的胶原凝胶收缩被认为是伤口修复反应和组织收缩的部分模型。在本研究中，我们通过逆转录聚合酶链反应（RT-PCR）和免疫细胞化学方法，在人胎儿肺成纤维细胞（HFL-1）上发现了激活素I型受体（ActR-I和ActR-IB）和II型受体（ActR-II）的表达。我们还研究了激活素A对HFL-1介导的胶原凝胶收缩的影响。激活素A以剂量依赖的方式刺激胶原凝胶收缩，其作用被一种特异性抑制激活素A活性的激活素结合蛋白卵泡抑素所消除。本研究表明，ActR-I、ActR-1B和ActR-II在人胎儿肺成纤维细胞上表达，且激活素A调节成纤维细胞介导的胶原凝胶收缩，提示激活素A可能参与了肺纤维化中观察到的人肺成纤维细胞活性和结构重塑。
