Creating a mouse model resistant to induced ischemic stroke and cardiovascular damage.

ABSTRACT: Vascular prostanoids, isomerized from an intermediate prostaglandin (PG), H₂, produced by cyclooxygenase (COX), exert various effects on the vascular system, both protective and destructive. During endothelial dysfunction, vascular protector prostacyclin/prostaglandin I₂ (PGI₂) is decreased, while inflammatory PGE₂ and thrombotic TXA₂ are increased. Therefore, our research aim was to reverse the event by controlling PGH₂ metabolism by generating an in vivo model via enzymatic engineering of COX-1 and prostacyclin synthase (PGIS). The COX-1 and PGIS genes were linked to a 10-residue amino acid linker to form a Single-chain Enzyme Complex (SCHEC), COX-1-10aa-PGIS. Transgenic (CP-Tg) mice in a FVB/N background were generated us

SUBMITTER: Ling QL 

PROVIDER: S-EPMC5786049 | biostudies-literature | 2018 Jan

REPOSITORIES: biostudies-literature