Stimulated neutrophils induce myosin light chain phosphorylation and isometric tension in endothelial cells
Stimulated neutrophils induce myosin light chain phosphorylation and isometric tension in endothelial cells
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DOI：
10.1152/ajpheart.1997.273.2.h981
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发表时间：
1997-08-01
影响因子：
4.8
通讯作者：
Huang, AJ
中科院分区：
文献类型：
--
作者：
Hixenbaugh, EA;Goeckeler, ZM;Huang, AJ
多形核白细胞（PMN）穿透相邻内皮细胞（EC）之间的连接以穿越内皮屏障的机制尚未解决。我们报告，趋化因子刺激的中性粒细胞诱导EC肌球蛋白调节轻链的丝氨酸19和苏氨酸18的磷酸化和EC单层的等距张力产生的协调增加。未受刺激的PMN对这两个参数都没有影响。这些发现，加上我们以前的报告（黄等人，J. Cell Biol.120：1371-1380，1993），即化学引诱物刺激的PMN引起EC胞质游离Ca 2+的升高，提供了强有力的推定证据，即肌球蛋白轻链激酶是EC酶，负责响应于化学引诱物刺激的PMN而引发肌球蛋白轻链磷酸化、EC收缩和等长张力产生。我们认为，通过诱导EC细胞骨架蛋白的磷酸化，趋化因子刺激的中性粒细胞诱导EC打开其细胞间连接，从而促进这些白细胞的跨内皮运动。
The mechanism or mechanisms by which polymorphonuclear leukocytes (PMN) penetrate junctions between neighboring endothelial cells (EC) to traverse endothelial barriers remain unresolved. We report that chemoattractant-stimulated PMN induce a coordinate increase in both phosphorylation of serine 19 and threonine 18 of EC myosin regulatory light chains and isometric tension generation by EC monolayers. Unstimulated PMN had no effect on either parameter. These findings, coupled with our previous report (Huang et al., J. Cell Biol. 120: 1371-1380, 1993) that chemoattractant-stimulated PMN cause a rise in EC cytosolic free Ca2+, provide strong presumptive evidence that myosin light chain kinase is the EC enzyme responsible for initiating myosin light chain phosphorylation, EC contraction, and isometric tension generation in response to chemoattractant stimulated PMN. We suggest that, by inducing phosphorylation of EC cytoskeletal proteins, chemoattractant-stimulated PMN induce EC to open their intercellular junctions, thereby facilitating transendothelial movement of these leukocytes.