Protective Role of mPGES-1 (Microsomal Prostaglandin E Synthase-1)-Derived PGE₂ (Prostaglandin E₂) and the Endothelial EP4 (Prostaglandin E Receptor) in Vascular Responses to Injury.

ABSTRACT:

Objective

Deletion of mPGES-1 (microsomal prostaglandin E synthase-1)-an anti-inflammatory target alternative to COX (cyclooxygenase)-2-attenuates injury-induced neointima formation in mice. This is attributable to the augmented levels of PGI₂ (prostacyclin)-a known restraint of the vascular response to injury, acting via IP (I prostanoid receptor). To examine the role of mPGES-1-derived PGE₂ (prostaglandin E₂) in vascular remodeling without the IP.

Approach and results

Mice deficient in both IP and mPGES-1 (DKO [double knockout] and littermate controls [IP KO (knockout)]) were subjected to angioplasty wire injury. Compared with the deletion of IP alone, coincident deletion of IP and mPGES-1 increased neointima formation, without affecting me

SUBMITTER: Hao H 

PROVIDER: S-EPMC5920701 | biostudies-literature | 2018 May

REPOSITORIES: biostudies-literature