Electric field down-regulates CD9 to promote keratinocytes migration through AMPK pathway
Electric field down-regulates CD9 to promote keratinocytes migration through AMPK pathway
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电场下调 CD9 通过 AMPK 途径促进角质形成细胞迁移
DOI：
10.7150/ijms.42840
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发表时间：
2020-01-01
影响因子：
3.6
通讯作者：
Jiang, Xupin
中科院分区：
文献类型：
--
作者：
Ji, Ran;Teng, Miao;Jiang, Xupin
内源性电场（EF）引导的角化细胞迁移已知在伤口再上皮化过程中起关键作用。尽管许多分子和信号通路对EF下角质形成细胞的定向迁移很重要，但潜在的机制尚不清楚。我们之前的研究发现，CD9是一种跨膜蛋白，参与创面再上皮化，CD9下调有助于角质形成细胞的迁移。在本研究中，我们观察了EF对CD9表达和角质形成细胞迁移的影响。EF （200mV/mm）作用下，角质形成细胞向阴极方向迁移，CD9表达下调。此外，CD9过表达逆转ef诱导的迁移速度和角化细胞的电致化反应。此外，我们发现EF降低了amp活化蛋白激酶（AMPK）的活性。此外，AMPK激活剂AICAR增加了EF下角质形成细胞中CD9的表达，而AMPK抑制剂化合物C则降低了CD9的表达。我们的研究结果表明，EF调节CD9的表达和角化细胞的定向迁移，其中AMPK通路起重要作用。
Endogenous electric field (EF)-directed keratinocytes migration is known to play a key role in the wound re-epithelialization process. Although many molecules and signaling pathways are reported important for directional keratinocytes migration under EF, the underlying mechanism remains unclear. Our previous research found that CD9, a trans-membrane protein, is involved in wound re-epithelialization and CD9 downregulation contributes to keratinocytes migration. In this study, we observed the effect of EF on CD9 expression and keratinocytes migration. The keratinocytes migrated directionally toward the cathode and CD9 expression was down-regulated under EF (200mV/mm). In addition, CD9 overexpression reversed EF-induced migratory speed and the electrotactic response of keratinocytes. Also, we found that EF reduced AMP-activated protein kinase (AMPK) activity. Furthermore, AICAR, an AMPK activator, increased CD9 expression under EF, while compound C, an AMPK inhibitor, decreased CD9 expression in keratinocytes. Our results demonstrate that EF regulates CD9 expression and keratinocytes directional migration, in which AMPK pathway plays an important role.