血管黏附分子1(VCAM-1)介导急性病毒性心肌炎小鼠CD34^+VLA-4^+骨髓来源细胞迁移至心肌组织

VCAM-1-mediated migration of CD34^+VLA-4^+ bone marrow derived cells into myocardial tissues in mice with acute viral myocarditis

目的探讨急性病毒性心肌炎小鼠在血管黏附分子1(VCAM-1)的作用下,CD34^+VLA-4^+细胞的动员和定植情况。方法流式细胞术检测CD34^+迟现抗原4(VLA-4)^+细胞在心肌组织、外周血中的变化;实时定量PCR、Western blot法分别检测心肌组织中VCAM-1 mRNA、蛋白的相对水平。结果与对照组比较,急性病毒性心肌炎小鼠心肌中CD34^+VLA-4^+细胞在第3天升高,第7天达到高峰,之后开始下降,第14天和第28天仍高于对照组;外周血中CD34^+VLA-4^+细胞第3天降低,之后开始升高,第7天达到高峰,随后下降,第14天和第28天仍高于对照组。急性病毒性心肌炎小鼠心肌中VCAM-1的mRNA和蛋白含量明显增加。动员到心肌中的CD34^+VLA-4^+细胞与急性病毒性心肌炎VCAM-1呈正相关。结论 VCAM-1促进CD34^+VLA-4^+细胞动员到心肌组织中。

Objective To analyze the migration and expression of CD34^＋ VLA-4^＋ cells under the induction of vascular cell adhesion molecule-1（ VCAM-1） in a murine model of acute viral myocarditis（ VMC）. Methods Frequency of CD34^＋VLA-4^＋ cells in the myocardial tissues and peripheral blood were examined by flow cytometry. The mRNA and protein of VCAM-1 in the myocardial tissues were analyzed by real-time quantitative PCR and Western blotting. Results In the acute VMC mice,CD34^＋VLA-4^＋cell population in the myocardial tissues significantly increased at day 3, peaked at day 7, and then decreased,but it was still higher than that in the control group at day 14 and 28. It decreased in the peripheral blood at day 3,and then increased to the peak at day 7,thereafter it decreased,but was still higher than that in the control group at day 14 and 28. We found a high expression of VCAM-1 in the myocardial tissues of the acute VMC mice,paralleling the mobilization of CD34^＋VLA-4^＋ cells in the myocardial tissues. Conclusion VCAM-1 promotes CD34^＋VLA-4^＋ cell mobilization into the damaged myocardial tissues.