S1PR1 VSM paper 2020

We investigated the effect of a selective S1PR type 1 ligand, ozanimod, on VSM phenotype expression and autophagy in primary human brain VSM cells following acute hypoxia plus glucose deprivation (HGD; in vitro ischemic-like injury). Cells were treated with ozanimod and exposed to normoxia or HGD.

Crystal violet staining, standard immunoblotting, and immunocytochemical labeling techniques assessed cellular morphology, vacuolization, phenotype, and autophagic state. We observed that HGD temporally decreased VSM cell viability and concomitantly increased vacuolization, both of which ozanimod reversed. HGD induced a simultaneous elevation and reduction in levels of pro- and anti-autophagic proteins respectfully, and ozanimod attenuated this response.