Molecular association of CD98, CD29, and CD147 critically mediates monocytic U937 cell adhesion.

Molecular association of CD98, CD29, and CD147 critically mediates monocytic U937 cell adhesion.
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DOI:
10.4196/kjpp.2016.20.5.515
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发表时间:
2016-09
期刊:
The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology
影响因子:
--
通讯作者:
Cho JY
Cho JY
中科院分区:
其他
文献类型:
--
作者:
Kim MY;Cho JY

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单核细胞的粘附事件代表了由趋化因子诱导的炎症反应中的重要步骤。β1-整合素CD 29是调节白细胞迁移和外渗的主要粘附分子。尽管已知有几种粘附分子是CD 29的调节因子,但CD 29与其调节粘附分子(如CD 98和CD 147)之间的分子相互作用尚未完全阐明。因此,在这项研究中,我们研究了这些分子是否在功能上,生化和细胞生物学相关的单核细胞U937细胞与聚集刺激和阻断抗体,以及酶抑制剂。CD 29、CD 98和CD 147(但不包括CD 43、CD 44和CD 82)的表面水平升高。通过将CD 29、CD 98和CD 147与聚集激活抗体连接而激活它们,触发了细胞-细胞粘附的诱导,并且对于CD 29-、CD 98-和CD 147-诱导的U937细胞聚集,对各种酶抑制剂和聚集阻断抗体的敏感性相似。这些分子和肌动蛋白细胞骨架之间的分子关联,证实了共聚焦显微镜和免疫沉淀。这些结果有力地表明,CD 29可能通过其生物化学和细胞调节因子,包括CD 98和CD 147,通过肌动蛋白细胞骨架进行调节。
Adhesion events of monocytes represent an important step in inflammatory responses induced by chemokines. The β1-integrin CD29 is a major adhesion molecule regulating leukocyte migration and extravasation. Although several adhesion molecules have been known as regulators of CD29, the molecular interactions between CD29 and its regulatory adhesion molecules (such as CD98 and CD147) have not been fully elucidated. Therefore, in this study, we examined whether these molecules are functionally, biochemically, and cell-biologically associated using monocytic U937 cells treated with aggregation-stimulating and blocking antibodies, as well as enzyme inhibitors. The surface levels of CD29, CD98, and CD147 (but not CD43, CD44, and CD82) were increased. The activation of CD29, CD98, and CD147 by ligation of them with aggregation-activating antibodies triggered the induction of cell-cell adhesion, and sensitivity to various enzyme inhibitors and aggregation-blocking antibodies was similar for CD29-, CD98-, and CD147-induced U937 cell aggregation. Molecular association between these molecules and the actin cytoskeleton was confirmed by confocal microscopy and immunoprecipitation. These results strongly suggest that CD29 might be modulated by its biochemical and cellular regulators, including CD98 and CD147, via the actin cytoskeleton.
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