mProX™ Human ROCK1 Stable Cell Line

Wang, Xuewen et al. "S1PR2/RhoA/ROCK1 pathway promotes inflammatory bowel disease by inducing intestinal vascular endothelial barrier damage and M1 macrophage polarization." Biochemical pharmacology vol. 201 (2022): 115077.
Vascular and immune dysfunctions are believed to play a role in the development of inflammatory bowel disease (IBD). However, the precise mechanisms underlying mucosal vascular endothelial barrier dysfunction and the shift in macrophage phenotype remain unclear. This study delved into the mechanistic involvement of sphingosine 1-phosphate receptor 2 (S1PR2) and its downstream G protein RhoA/Rho kinase 1 (ROCK1) signaling pathway in IBD-associated intestinal endothelial barrier damage and M1 macrophage polarization. The research revealed significantly elevated S1PR2 expression in intestinal mucosal vascular endothelial cells and macrophages of IBD patients, DSS-induced colitis mice, and in vitro models subjected to LPS treatment. Knockdown or pharmacological inhibition of S1PR2 led to substantial downregulation of RhoA and ROCK1 in vascular endothelial cells and macrophages. Additionally, inhibiting S1PR2 and ROCK1 reversed vascular barrier dysfunction and M1 macrophage polarization both in vivo and in vitro, while mitigating endoplasmic reticulum (ER) stress in vascular endothelial cells and glycolysis in macrophages. Furthermore, inhibition of ER stress or glycolysis countered LPS-induced impairment of vascular endothelial cell barrier function and M1 macrophage polarization. In conclusion, these findings suggest that the S1PR2/RhoA/ROCK1 signaling pathway could be implicated in IBD pathogenesis by modulating vascular endothelial barrier function and M1 macrophage polarization.
Wang, Xuewen et al. "S1PR2/RhoA/ROCK1 pathway promotes inflammatory bowel disease by inducing intestinal vascular endothelial barrier damage and M1 macrophage polarization." Biochemical pharmacology vol. 201 (2022): 115077.
Pubmed: 35537530   DOI: 10.1016/j.bcp.2022.115077

Chi, Zengpeng. et al. "Silencing geranylgeranyltransferase I inhibits the migration and invasion of salivary adenoid cystic carcinoma through RhoA/ROCK1/MLC signaling and suppresses proliferation through cell cycle regulation." Cell biology international, 2023.
In the study, the researchers aimed to investigate the impact and mechanism of Geranylgeranyltransferase type I (GGTase-I) on the malignant progression of salivary adenoid cystic carcinoma (SACC). GGTase-I, known to affect Rho proteins, has been linked to the development of several cancers. The study utilized short hairpin RNA-EGFP-lentivirus to stably knock down the GGTase-I gene in cells. The effects of GGTase-I silencing on different aspects of SACC cells, such as migration, invasion, and spread, were examined. The study also assessed the expression levels of GGTase-I and RhoA genes and proteins, as well as potential underlying mechanisms involving proteins such as ROCK1, MLC, p-MLC, E-cadherin, Vimentin, MMP2, MMP9, cyclinD1, MYC, E2F1, and p21.
Chi, Zengpeng. et al. "Silencing geranylgeranyltransferase I inhibits the migration and invasion of salivary adenoid cystic carcinoma through RhoA/ROCK1/MLC signaling and suppresses proliferation through cell cycle regulation." Cell biology international, 2023.
Pubmed: 37853939   DOI: 10.1002/cbin.12096