Ding B, Huang S L, Zhang S Q, Li Y X
Laboratory of Molecular Pharmacology, Hu-nan Medical University, Changsha 410078, China.
Acta Pharmacol Sin. 2000 Feb;21(2):174-8.
To investigate whether the effect of angiotensin (Ang) II or epidermal growth factor (EGF) on cardiac fibroblast proliferation involved in activation of extracellular signal-regulated kinase (ERK) 1/2 or Ca(2+)-calmodulin dependent protein kinase(CCDPK) mediated by protein kinase C (PKC)-zeta.
Relative activity of CCDPK was measured by Western blotting. DNA synthesis was assayed by [3H]thymidine incorporation.
PDBU caused no decrease in Ang II- and 10% FCS-stimulated CCDPK activity and DNA synthesis. In contrary, 65% or 75% EGF- or tetradecanoylphorbol acetate (TDPA, formally called PMA)--stimulated CCDPK activity and 38% or 42% [3H]thymidine incorporation treated by PDBU were inhibited, respectively. Meanwhile 70% and 72% CCDPK activities induced by Ang II and EGF were inhibited by PD 98059, respectively.
PKC-zeta mediated Ang II-induced activation of CCDPK and cardiac fibroblast proliferation.
研究血管紧张素（Ang）II或表皮生长因子（EGF）对心脏成纤维细胞增殖的影响是否涉及由蛋白激酶C（PKC）-ζ介导的细胞外信号调节激酶（ERK）1/2或钙调蛋白依赖性蛋白激酶（CCDPK）的激活。
通过蛋白质印迹法测量CCDPK的相对活性。通过[3H]胸腺嘧啶核苷掺入法测定DNA合成。
佛波醇-12，13-二丁酸酯（PDBU）未使Ang II和10%胎牛血清（FCS）刺激的CCDPK活性及DNA合成降低。相反，PDBU处理分别抑制了65%或75%的EGF或十四酰佛波醇乙酸酯（TDPA，原称为PMA）刺激的CCDPK活性以及38%或42%的[3H]胸腺嘧啶核苷掺入。同时，PD 98059分别抑制了Ang II和EGF诱导的70%和72%的CCDPK活性。
PKC-ζ介导Ang II诱导的CCDPK激活及心脏成纤维细胞增殖。
