Role of MLC<sub>20</sub> phosphorylation in PKCα and PKCε  regulating  calcium sensitivity in cultured hypoxic VSMCs and in hemorrhagic shock rats

徐竞; 杨光明; 李涛; 明佳; 陈玮; 张瑗; 刘良明

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Role of MLC₂₀ phosphorylation in PKCα and PKCε regulating calcium sensitivity in cultured hypoxic VSMCs and in hemorrhagic shock rats

更新时间：2026-01-09

- Role of MLC₂₀ phosphorylation in PKCα and PKCε regulating calcium sensitivity in cultured hypoxic VSMCs and in hemorrhagic shock rats
- Journal of Army Medical University Vol. 30, Issue 21, Pages: 1972-1975(2008)
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  CLC： R363;R345.57;R605.971
- Published：2008
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徐竞,杨光明,李涛,明佳,陈玮,张瑗,刘良明.MLC20磷酸化在PKCα、PKCε调节失血性休克大鼠血管钙敏感性中的作用[J].陆军军医大学学报(原第三军医大学学报),2008,30(21):1972-1975.

　XU Jing,YANG Guang-ming,LI Tao,MING Jia,CHEN Wei,ZHANG Yuan,LIU Liang-ming.Role of MLC20 phosphorylation in PKCα and PKCε regulating calcium sensitivity in cultured hypoxic VSMCs and in hemorrhagic shock rats[J].J Amry Med Univ (J Third Mil Med Univ),2008,30(21):1972-1975.
徐竞,杨光明,李涛,明佳,陈玮,张瑗,刘良明.MLC20磷酸化在PKCα、PKCε调节失血性休克大鼠血管钙敏感性中的作用[J].陆军军医大学学报(原第三军医大学学报),2008,30(21):1972-1975. DOI：

　XU Jing,YANG Guang-ming,LI Tao,MING Jia,CHEN Wei,ZHANG Yuan,LIU Liang-ming.Role of MLC20 phosphorylation in PKCα and PKCε regulating calcium sensitivity in cultured hypoxic VSMCs and in hemorrhagic shock rats[J].J Amry Med Univ (J Third Mil Med Univ),2008,30(21):1972-1975. DOI：

摘要

目的观察肌球蛋白轻链（MLC

）磷酸化在蛋白激酶Cα（protein kinase Cα

PKCα）、蛋白激酶Cε（protein kinase Cε

PKCε）调节大鼠失血性休克后血管钙敏感性中的作用，进一步探讨休克血管钙失敏的发生机制。方法采用缺氧大鼠血管平滑肌细胞（vascular smooth muscle cell，VSMC）和失血性休克后大鼠肠系膜上动脉（superior mesenteric artery，SMA），运用Western blot、底物磷酸化等技术方法，观察PKCα、PKCε激动剂作用下，以及抑制CPI-17、ILK、ZIPK后再给予PKCα、PKCε激动剂时，肌球蛋白轻链磷酸酶（myosin light chain phosphatase，MLCP）活性和MLC

磷酸化的变化。结果 ①缺氧2 h后VSMC中MLCP活性增高至正常对照的150.1％（P0.01），PKCα、PKCε激动剂可显著抑制其增高，使其分别降低至正常对照的103.0％和96.3％（P0.01），抑制CPI-17、ILK、ZIPK，可显著抑制PKCα激动剂降低MLCP活性的作用，使其分别增高至正常对照的136.7％、127.6％和116.7％（P0.01）；抑制CPI-17、ILK、ZIPK，也可显著抑制PKCε激动剂降低MLCP活性的作用，使其分别增高至134.0％、128.5％和126.0％（P0.01）。②失血性休克2 h后SMA中MLC

磷酸化水平由32.4%显著降低至10.4%（P0.01），PKCα、PKCε激动剂可显著抑制其降低，使其分别增高至26.4%和25.6%（P0.01），抑制CPI-17、ILK、ZIPK，可显著削弱PKCα激动剂的增高MLC

磷酸化的作用，使其分别降低至12.7%、10.0%和15.7%（P0.01）；也可显著削弱PKCε激动剂增高MLC

磷酸化的作用，使其分别降低至10.1%、12.5%和10.3%（P0.01）。结论 PKCα、PKCε可能通过CPI-17、ILK、ZIPK调节MLCP活性和MLC

磷酸化，调节失血性休克血管平滑肌的钙敏感性。

Abstract

jective To observe the role of 20 kDa myosin light chain (MLC

) phosphorylation in the regulation of protein kinase Cα (PKCα) and PKCε on calcium sensitivity during hemorrhagic shock (HS) in rats for the mechanism of calcium desensitization. Methods Vascular smooth muscle cells (VSMCs) after hypoxia and superior mesenteric artery (SMA) from HS rats were adopted to observe the effects of PKCα and PKCε agonists on the activity of myosin light chain phosphatase (MLCP) and the phosphorylation of MLC

and observe the influence of inhibitors of PKC-potentiated inhibitory protein for protein phosphatase 1 of 17 kDa (CPI-17)

integrin-linked kinase (ILK) and zipper-interacting protein kinase (ZIPK) on the action of PKCα and PKCε agonists in these events by Western blotting and substrate phosphorylation. Results (1) MLCP activity was increased to 150.1％ of normal control group in VSMC after 2 h hypoxia (P0.01)

and was decreased to 103.0％ (P0.01) or 96.3％(P0.01) by PKCα agonist or PKCε agonist. Comparing with PKCα agonist group

MLCP activity was increased to 136.7％ (P0.01)

127.6％ (P0.01) and 116.7％ (P0.01) after the treatment of the inhibitors of CPI-17

ILK and ZIPK respectively. Comparing with PKCε agonist group

MLCP activity was increased to 134.0％(P0.01)

128.5％ (P0.01) and 126.0％ (P0.01) respectively by the inhibitors of CPI-17

ILK and ZIPK. (2) MLC

phosphorylation was decreased from 32.4% to 10.4% (P0.01) in SMA after 2 h shock

and was increased to 26.4% (P0.01) and 25.6% (P0.01) by PKCα and PKCε agonists. Comparing with PKCα agonist group

MLC

phosphorylation was decreased to 12.7% (P0.01)

10.0% (P0.01) and 15.7% (P0.01) respectively by the inhibitors of CPI-17

ILK and ZIPK. Comparing with PKCε agonist group

MLC

phosphorylation was decreased to 10.1% (P0.01)

12.5% (P0.01) and 10.3% (P0.01) respectively by the inhibitors of CPI-17

ILK and ZIPK. Conclusion PKCα and PKCε may regulate the MLCP activity and MLC

phosphorylation via CPI-17

ILK and ZIPK

to modulate calcium sensitization of vascular smooth muscle following HS.

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Role of MLC20 phosphorylation in PKCα and PKCε regulating calcium sensitivity in cultured hypoxic VSMCs and in hemorrhagic shock rats

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Role of MLC₂₀ phosphorylation in PKCα and PKCε regulating calcium sensitivity in cultured hypoxic VSMCs and in hemorrhagic shock rats