期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 23, 期 18, 页码 -出版社
MDPI
DOI: 10.3390/ijms231810932
关键词
lysophosphatidylinositol; GPR55; endocannabinoid; lysophospholipid mediator; morphological change; G(12 13)-RhoA-ROCK pathway
资金
- Ministry of Education, Culture, Sports, Sciences, and Technology of Japan [21590075, 24590095, 15K07946, 19K07088, 22K06584]
This study found that LPI induced morphological changes and cytoskeleton rearrangement in GPR55-expressing HEK293 cells, which was mediated through the GPR55-RhoA-ROCK signaling pathway.
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.
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