Faculty of Pharma-Science, Teikyo University, 2-11-1 Kaga, Itabashi-ku, Tokyo 173-8605, Japan.
Pharmaceutical Department, Teikyo University Hospital, 2-11-1 Kaga, Itabashi-ku, Tokyo 173-8606, Japan.
Int J Mol Sci. 2022 Sep 18;23(18):10932. doi: 10.3390/ijms231810932.
We previously reported that lysophosphatidylinositol (LPI) functions as an endogenous agonist of GPR55, a novel cannabinoid receptor. However, the physiological roles of LPI-GPR55 have not yet been elucidated in detail. In the present study, we found that LPI induced morphological changes in GPR55-expressing HEK293 cells. LPI induced the cell rounding of GPR55-expressing HEK293 cells but not of empty-vector-transfected cells. LPI also induced the activation of small GTP-binding protein RhoA and increased stress fiber formation in GPR55-expressing HEK293 cells. The inhibition of RhoA and Rho kinase ROCK by the C3 exoenzyme and the ROCK inhibitor reduced LPI-induced cell rounding and stress fiber formation. These results clearly indicated that the LPI-induced morphological changes and the assembly of the cytoskeletons were mediated through the GPR55-RhoA-ROCK pathway.
我们之前报道过溶血磷脂酰肌醇 (LPI) 作为新型大麻素受体 GPR55 的内源性激动剂发挥作用。然而，LPI-GPR55 的生理作用尚未详细阐明。在本研究中，我们发现 LPI 诱导表达 GPR55 的 HEK293 细胞发生形态变化。LPI 诱导表达 GPR55 的 HEK293 细胞发生细胞圆化，但不诱导空载体转染细胞发生细胞圆化。LPI 还诱导小 G 蛋白 RhoA 的激活，并增加表达 GPR55 的 HEK293 细胞中的应力纤维形成。C3 外切酶和 ROCK 抑制剂对 RhoA 和 Rho 激酶 ROCK 的抑制作用降低了 LPI 诱导的细胞圆化和应力纤维形成。这些结果清楚地表明，LPI 诱导的形态变化和细胞骨架的组装是通过 GPR55-RhoA-ROCK 途径介导的。
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