Abstract:
BACKGROUND:Microsomal (m) prostaglandin (PG) E₂ synthase (S)-1 catalyzes the formation of PGE₂ from PGH₂, a cyclooxygenase product that is derived from arachidonic acid. Previous studies in mice suggest that targeting mPGES-1 may be less likely to cause hypertension or thrombosis than cyclooxygenase-2-selective inhibition or deletion in vivo. Indeed, deletion of mPGES-1 retards atherogenesis and angiotensin II-induced aortic aneurysm formation. The role of mPGES-1 in the response to vascular injury is unknown. METHODS AND RESULTS:Mice were subjected to wire injury of the femoral artery. Both neointimal area and vascular stenosis were significantly reduced 4 weeks after injury in mPGES-1 knockout mice compared with wild-type controls (65.6 ± 5.7 versus 37.7 ± 5.1 × 10³ pixel area and 70.5 ± 13.4% versus 47.7 ± 17.4%, respectively; P < 0.01). Induction of tenascin-C, a proproliferative and promigratory extracellular matrix protein, after injury was attenuated in the knockouts. Consistent with in vivo rediversion of PG biosynthesis, mPGES-1-deleted vascular smooth muscle cells generated less PGE₂ but more PGI₂ and expressed reduced tenascin-C compared with wild-type cells. Both suppression of PGE₂ and augmentation of PGI₂ attenuate tenascin-C expression and vascular smooth muscle cell proliferation and migration in vitro. CONCLUSIONS:Deletion of mPGES-1 in mice attenuates neointimal hyperplasia after vascular injury, in part by regulating tenascin-C expression. This raises for consideration the therapeutic potential of mPGES-1 inhibitors as adjuvant therapy for percutaneous coronary intervention.
journal_name
Circulationjournal_title
Circulationauthors
Wang M,Ihida-Stansbury K,Kothapalli D,Tamby MC,Yu Z,Chen L,Grant G,Cheng Y,Lawson JA,Assoian RK,Jones PL,Fitzgerald GAdoi
10.1161/CIRCULATIONAHA.110.973685subject
Has Abstractpub_date
2011-02-15 00:00:00pages
631-9issue
6eissn
0009-7322issn
1524-4539pii
CIRCULATIONAHA.110.973685journal_volume
123pub_type
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