Antagonistic regulation of protein kinase C‐induced stimulation of fibronectin synthesis by cyclic AMP in human lung fibroblasts
Antagonistic regulation of protein kinase C‐induced stimulation of fibronectin synthesis by cyclic AMP in human lung fibroblasts
复制标题
人肺成纤维细胞中环AMP对蛋白激酶C诱导的纤连蛋白合成刺激的拮抗调节
DOI：
10.1080/15216549700204171
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发表时间：
1997
期刊：
影响因子：
--
通讯作者：
In‐San Kim
中科院分区：
文献类型：
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作者：
Byungheon Lee;R. Park;K. Sohn;In‐San Kim
我们研究了cAMP和蛋白激酶C（PKC）信号通路在人肺成纤维细胞纤连蛋白合成调控中的相互作用。佛波醇肉豆蔻酸酯（PMA），一种PKC激活剂，刺激正常和转化的人肺成纤维细胞（分别为WI-38和WI-38 VA 13）中的纤连蛋白合成及其mRNA表达。另一方面，二丁酰cAMP（Bt 2cAMP），cAMP类似物，并没有改变纤连蛋白的合成在这两个细胞系。然而，Bt 2cAMP与PMA的联合处理抑制了PMA诱导的这些细胞中纤连蛋白合成和mRNA表达的刺激。本研究表明cAMP通路在调节人肺成纤维细胞纤连蛋白合成中拮抗PKC通路，为cAMP和PKC信号通路之间的拮抗相互作用提供了一个实例。
We studied the interaction between cAMP and protein kinase C (PKC) signaling pathways in the regulation of fibronectin synthesis in human lung fibroblasts. Phorbol myristate acetate (PMA), a PKC activator, stimulated fibronectin synthesis and its mRNA expression in both normal and transformed human lung fibroblasts (WI‐38 and WI‐38 VA13, respectively). On the other hand, dibutyryl cAMP (Bt2cAMP), a cAMP analogue, did not alter fibronectin synthesis in both cell lines. The combined treatment of Bt2cAMP with PMA, however, suppressed the PMA‐induced stimulation of fibronectin synthesis and mRNA expression in these cells. This study shows that cAMP pathway antagonizes PKC pathway in regulating fibronectin synthesis in human lung fibroblasts and provides an example of antagonistic interaction between cAMP and PKC signaling pathways.