PTGS2
LOCUS ID5743
GENE_SYMBOLPTGS2
GENE NAMEprostaglandin-endoperoxide synthase 2 (prostaglandin G/H synthase and cyclooxygenase)
SYNONYMNSCOX2, COX-2, PHS-2, PGG/HS, PGHS-2, hCox-2, GRIPGHS
CHROMOSOME1
HOMOLOGENE ID31000
microRNAsNANA
GENE SUMMARY
Prostaglandin-endoperoxide synthase (PTGS), also known as cyclooxygenase, is the key enzyme in prostaglandin biosynthesis, and acts both as a dioxygenase and as a peroxidase. There are two isozymes of PTGSa constitutive PTGS1 and an inducible PTGS2, which differ in their regulation of expression and tissue distribution. This gene encodes the inducible isozyme. It is regulated by specific stimulatory events, suggesting that it is responsible for the prostanoid biosynthesis involved in inflammation and mitogenesis. [provided by RefSeq, Feb 2009]

OBSERVATIONS

Complication Evidence PMID
Nephropathy1. Losartan could suppress the expression of COX2 and TGF-beta1 in the kidney of DN rats and attenuate the renal lesions caused by DN.18812657
Cardiovascular1. Specifically, SILD1) normalizes the frequency of circulating pro-inflammatory monocytes triggered by hyperglycemia (53.7 +- 7.9% of CD11b+Gr-1+ cells in STZ vs. 30.4 +- 8.3% in STZ+SILD and 27.1 +- 1.6% in CTRL, P<0.01); 2) prevents STZ-induced tissue inflammatory infiltration (4-fold increase in F4/80+ macrophages in diabetic vs. control mice) by increasing renal and heart anti-inflammatory TEMs (30.9 +- 3.6% in STZ+SILD vs. 6.9 +- 2.7% in STZ, P <0.01, and 11.6 +- 2.9% in CTRL mice); 3) reduces vascular inflammatory proteins (iNOS, COX2, VCAM-1) promoting tissue protection; 4) lowers monocyte adhesion to human endothelial cells in vitro through the TIE2 receptor. All these changes occurred independently from changes of glycemic status.25961566
Retinopathy1. COX-2 contributes markedly to preretil neovascularization in ischemic retinopathies, and this effect seems to be Prostaglangin E2 (PGE2) mediated mostly via EP3receptors implicating a new interaction through TSP-1 and CD3612821538
Neuropathy1. These prelimiry data support the role of the activation of the COX-2 pathway in mediating sensory and motor nerve conduction velocity deficits in experimental diabetic neuropathy (EDN). These findings also suggest that the COX-2 pathway seems to be an important modulator of oxidative stress in EDN.16356116