Lysophosphatidylinositol Induced Morphological Changes and Stress Fiber Formation through the GPR55-RhoA-ROCK Pathway

  • Int J Mol Sci. 2022 Sep 18;23(18):10932. doi: 10.3390/ijms231810932.
Keisuke Nakajima  1  2 ,  Saori Oka  1 ,  Takashi Tanikawa  3 ,  Yoko Nemoto-Sasaki  1 ,  Naoki Matsumoto  1 ,  Hiroki Ishiguro  4 ,  Yoichiro Arata  1 ,  Takayuki Sugiura  1 ,  Atsushi Yamashita  1
Affiliations
  • 1. Faculty of Pharma-Science, Teikyo University, 2-11-1 Kaga, Itabashi-ku, Tokyo 173-8605, Japan.
  • 2. Pharmaceutical Department, Teikyo University Hospital, 2-11-1 Kaga, Itabashi-ku, Tokyo 173-8606, Japan.
  • 3. Faculty of Pharmacy and Pharmaceutical Sciences, Josai University, 1-1 Keyakidai, Sakado 350-0295, Japan.
  • 4. Department of Clinical Genetics, Graduate School of Medicine, University of Yamanashi, 1110, Shimokato, Chuo-shi 409-3821, Japan.
PMID: 36142844 DOI: 10.3390/ijms231810932
Abstract

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.

Keywords
G12/13-RhoA-ROCK pathway; GPR55; endocannabinoid; lysophosphatidylinositol; lysophospholipid mediator; morphological change.
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