| 朱彬 孙强 张鹭鹭 刘惊今 姜苗苗
王帆 卢少玲 孟玮 白景玉 张烁.ERK信号通路对病毒性心肌炎心肌细胞CAR 表达的影响[J].现代生物医学进展英文版,2015,15(25):4828-4833. |
| ERK信号通路对病毒性心肌炎心肌细胞CAR 表达的影响 |
| Roles of ERK Signal Transduction Pathway to Coxsackie-adenovirusReceptor (CAR) in Cardiocytes during Viral Myocarditis |
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| DOI： |
| 中文关键词: 病毒性心肌炎 ERK1/2 CAR |
| 英文关键词: Viral myocarditis ERK1/2 Coxsackievirus-adenovirus receptor |
| 基金项目:黑龙江省教育厅科学技术研究项目（115811176） |
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| 中文摘要: |
| 目的：观察细胞外信号调节激酶（Extracellular Regulated Protein Kinases, ERK1/2）信号通路对病毒性心肌炎（Viral
Myocarditis, VMC）心肌细胞柯萨奇病毒- 腺病毒受体（Coxsackie-adenovirus Receptor, CAR）表达的影响。方法：新生SD大鼠心肌
细胞体外培养48 h后随机分为3 组，除对照组外均体外接种柯萨奇B3m病毒（Coxsackievirus B, CVB），建立VMC 细胞模型。C
组：DMEM对照组；V 组：CVB3m感染组；U+V 组：接种病毒前30 min，给予ERK1/2 通路抑制剂U0126（10 滋mol/L）。各组分别于
种毒后12 h、24 h、36 h取心肌细胞，用Western blot 法测定ERK1/2 活化水平及CAR表达量，并按上述时间点观察各组心肌细胞
形态、搏动情况、细胞损伤程度，取培养液测定乳酸脱氢酶（LDH）水平。结果: 在接种病毒后12 h，V 组与C组相比，P-ERK1/2 表
达增高（3.25± 0.61 vs 0.59± 0.09，P<0.05），CAR表达增高（1.03± 0.17 vs 0.78± 0.11，P>0.05），逐步出现细胞病变，细胞搏动停止，
培养液中LDH水平明显增高（1016.67± 67.75 vs 336.34± 28.67，P<0.05），心肌酶学的升高与镜下心肌细胞损伤程度平行；U+V 组
与V 组相比，P-ERK1/2 表达降低（1.66± 0.28 vs 3.25± 0.61，P<0.05），CAR表达明显增高（1.73± 0.27 vs 1.03± 0.17，P<0.05），但细
胞损伤却明显减轻，LDH 水平明显降低（410.06± 13.62 vs 1016.67± 67.75，P<0.05）。动态观察24 h、36 h，同样出现上述变化趋势。
结论：ERK1/2 信号转导通路参与心肌细胞感染CVB 发生急性损伤的过程，并参与调控CAR 的表达。在病毒感染后36 h内，阻断
ERK1/2 信号通路，CAR表达上调，并未加重心肌细胞损伤。 |
| 英文摘要: |
| Objective:To investigate the role of extracellular signal-regulated kinase (ERK) signal transduction pathway to
coxsackie-adenovirus receptor (CAR) in cardiocytes during viral myocarditis (VMC).Methods:Primary cultured new born SD rat
cardiocytes were infected by CVB3m to establish a model of viral myocarditis. Forty-eight hours after culturing, cardiomyocytes were
divided into 3 groups. Group C: cardiomyocytes were incubated with DMEM as controls; group V: cardiomyocytes were incubated with
CVB solutions; group U+V: cardiomyocytes were incubated with U0126 (10 umol/L) for 30 min initially, and then incubated with CVB
solutions. After processing, the level of P-ERK1/2 and CAR were detected by Western blot. CVB mediated cytopathic effects were
observed after co-culturing for further 12, 24, 36 hours respectively, lesions of the cardiocytes were examined by LDH assay.Results:Twelve hous after infected by CVB, comparing to group C, the level of P-ERK1/2 in group V increased (3.25± 0.61 vs 0.59± 0.09, P<0.
05), the exrpession of CAR increased (1.03± 0.17 vs 0.78± 0.11, P>0.05), the beating rate decreased gradually and then stopped, the
level of cardiac enzymes increased (1016.67± 67.75 vs 336.34± 28.67, P<0.05). In group U+V, comparing to group V, the level of
P-ERK1/2 decreased (1.66± 0.28 vs 3.25± 0.61, P<0.05), the exrpession of CAR increased significantly (1.73± 0.27 vs 1.03± 0.17, P<0.
05), the injury to cardiocyte extenuates, so was the level of cardiac enzymes (410.06± 13.62 vs 1016.67± 67.75, P<0.05). During the
following 24 and 36 hours, we can also observe the same change.Conclusion:When cardiocytes were infected by CVB3m in acute
phase, ERK1/2 signal transduction pathway was involved in it. It also participated in the regulation of CAR. Inhibition of this pathway
did not aggravate the injury of cardiac cells. |
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