Protein kinase regulation of tumor necrosis factor alpha stimulated collagenase and stromelysin message levels in chondrocytes.
Protein kinase regulation of tumor necrosis factor alpha stimulated collagenase and stromelysin message levels in chondrocytes.
复制标题
肿瘤坏死因子α的蛋白激酶调节刺激软骨细胞中的胶原酶和溶基质素信息水平。
DOI：
10.1006/bbrc.1993.2369
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发表时间：
1993
影响因子：
3.1
通讯作者：
Cheung,HS
中科院分区：
文献类型：
--
作者：
Mitchell,PG;Cheung,HS
TNF 刺激猪关节软骨细胞中金属蛋白酶胶原酶和溶基质素的转录和分泌。 TNF 诱导的金属蛋白酶转录可以通过蛋白激酶抑制剂（H7 或十字孢菌素）或通过提高细胞内 cAMP 水平来抑制。 HA1004 是一种蛋白激酶抑制剂，其结构与 H7 相关，但对蛋白激酶 C 的 Ki 较高，对 TNF 诱导的信息水平没有影响。软骨细胞的 TNF 处理不会诱导膜相关的 PKC 或增加细胞内 cAMP 水平。我们的结果与软骨细胞中 TNF 信号转导中与 PKC 不同的星形孢菌素和 H7 敏感蛋白激酶的参与一致。
TNF stimulated transcription and secretion of the metalloproteinases collagenase and stromelysin in porcine articular chondrocytes. TNF induced metalloproteinase transcription could be inhibited with either protein kinase inhibitors (H7 or staurosporine) or by raising intracellular cAMP levels. HA1004, a protein kinase inhibitor structurally related to H7 but with a higher Ki for protein kinase C had no effect on TNF induced message levels. TNF treatment of chondrocytes did not induce membrane associated PKC or increase intracellular cAMP levels. Our results are consistent with the involvement of a staurosporine and H7 sensitive protein kinase distinct from PKC in TNF signal transduction in chondrocytes.