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Mechanical stiffness softening and cell adhesion are coordinately regulated by ERM dephosphorylation in KG-1 cells
Human Cell ( IF 3.4 ) Pub Date : 2021-07-26 , DOI: 10.1007/s13577-021-00584-2
Takanori Kihara 1 , Teru Matsumoto 1 , Yoshihito Nakahashi 1 , Kouichi Tachibana 2, 3
Affiliation  

Mechanical stiffness is closely related to cell adhesion and rounding in some cells. In leukocytes, dephosphorylation of ezrin/radixin/moesin (ERM) proteins is linked to cell adhesion events. To elucidate the relationship between surface stiffness, cell adhesion, and ERM dephosphorylation in leukocytes, we examined the relationship in the myelogenous leukemia line, KG-1, by treatment with modulation drugs. KG-1 cells have ring-shaped cortical actin with microvilli as the only F-actin cytoskeleton, and the actin structure constructs the mechanical stiffness of the cells. Phorbol 12-myristate 13-acetate and staurosporine, which induced cell adhesion to fibronectin surface and ERM dephosphorylation, caused a decrease in surface stiffness in KG-1 cells. Calyculin A, which inhibited ERM dephosphorylation and had no effect on cell adhesion, did not affect surface stiffness. To clarify whether decreasing cell surface stiffness and inducing cell adhesion are equivalent, we examined KG-1 cell adhesion by treatment with actin-attenuated cell softening reagents. Cytochalasin D clearly diminished cell adhesion, and high concentrations of Y27632 slightly induced cell adhesion. Only Y27632 slightly decreased ERM phosphorylation in KG-1 cells. Thus, decreasing cell surface stiffness and inducing cell adhesion are not equivalent, but these phenomena are coordinately regulated by ERM dephosphorylation in KG-1 cells.



中文翻译:

KG-1细胞中ERM去磷酸化协同调节机械刚度软化和细胞粘附

机械刚度与某些细胞中的细胞粘附和变圆密切相关。在白细胞中,ezrin/radixin/moesin (ERM) 蛋白的去磷酸化与细胞粘附事件有关。为了阐明白细胞表面硬度、细胞粘附和 ERM 去磷酸化之间的关系,我们通过调节药物治疗检查了髓性白血病系 KG-1 中的关系。KG-1细胞具有环状皮质肌动蛋白,微绒毛是唯一的F-肌动蛋白细胞骨架,肌动蛋白结构构成细胞的机械刚度。Phorbol 12-myristate 13-acetate 和 staurosporine 可诱导细胞粘附到纤连蛋白表面和 ERM 去磷酸化,导致 KG-1 细胞的表面刚度降低。Calyculin A,抑制 ERM 去磷酸化,对细胞粘附没有影响,不影响表面刚度。为了阐明降低细胞表面刚度和诱导细胞粘附是否等效,我们通过用肌动蛋白减弱的细胞软化试剂处理检查了 KG-1 细胞粘附。Cytochalasin D 明显减少细胞粘附,高浓度的 Y27632 轻微诱导细胞粘附。只有 Y27632 略微降低了 KG-1 细胞中的 ERM 磷酸化。因此,降低细胞表面硬度和诱导细胞粘附并不等同,但这些现象是由 KG-1 细胞中的 ERM 去磷酸化协同调节的。和高浓度的 Y27632 轻微诱导细胞粘附。只有 Y27632 略微降低了 KG-1 细胞中的 ERM 磷酸化。因此,降低细胞表面硬度和诱导细胞粘附并不等同,但这些现象是由 KG-1 细胞中的 ERM 去磷酸化协同调节的。和高浓度的 Y27632 轻微诱导细胞粘附。只有 Y27632 略微降低了 KG-1 细胞中的 ERM 磷酸化。因此,降低细胞表面硬度和诱导细胞粘附并不等同,但这些现象是由 KG-1 细胞中的 ERM 去磷酸化协同调节的。

更新日期:2021-07-27
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