We are analyzing https://link.springer.com/article/10.1007/s00395-010-0129-9.

Title:
Effect of PAR2 in regulating TNF-α and NAD(P)H oxidase in coronary arterioles in type 2 diabetic mice | Basic Research in Cardiology
Description:
Protease-activated receptor-2 (PAR2) is expressed in endothelial cells and mediates endothelium-dependent vasodilation. We hypothesized that PAR2 regulates tumor necrosis factor-alpha (TNF-α)-induced coronary arteriolar dysfunction in type 2 diabetic (db/db) mice. To test this, coronary arterioles from WT control, db/db, db/db mice treated with PAR2 antagonist FSLLRY–NH2 (db/db+FSLLRY–NH2) and db/db mice null for TNF (dbTNF−/dbTNF−) were isolated and pressurized (60 cmH2O) without flow. Although vasodilation to the endothelium-independent vasodilator sodium nitroprusside (SNP) was not different among WT, db/db, db/db+FSLLRY–NH2 and dbTNF−/dbTNF−, endothelium-dependent acetylcholine (ACh)- and flow-mediated vasodilation were impaired in db/db mice but were enhanced in dbTNF−/dbTNF− mice and db/db mice treated with PAR2 antagonist. NOS inhibitor N G-nitro-l-arginine-methyl ester (l-NAME) significantly reduced ACh-induced dilation in WT, dbTNF−/dbTNF− and db/db+FSLLRY–NH2, but did not alter the vasodilation in db/db mice. In contrast, cyclooxygenase (COX) inhibitor indomethacin (Indo) did not alter ACh-induced vasodilation in these four groups of mice. PAR2-activating peptide (PAR2-AP, 2-Furoyl-LIGRLO-am)-induced dilation was higher in db/db mice than that in WT, dbTNF−/dbTNF− and db/db mice treated with PAR2 antagonist. These effects were abolished by denudation, or in the presence of l-NAME or Indo. Protein expressions of TNF-α, PAR2, gp91phox and p47phox in the heart and isolated coronary arterioles were higher in db/db mice compared to WT mice. Administration of PAR2 antagonist to db/db mice reduced protein expression of TNF-α, gp91phox and PAR2. Protein expression of gp91phox and p47phox was lower in dbTNF−/dbTNF− compared to db/db mice. These results indicate that PAR2 plays a pivotal role in endothelial dysfunction in type 2 diabetes by up-regulating the expression/production of TNF-α and activating NAD(P)H oxidase subunit p47phox.
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Topics {✒️}

g-nitro-l-arginine-methyl ester month download article/chapter xiaonai chen & cuihua zhang hdl receptor sr-b1 mediates endothelium-dependent vasodilation low-grade systemic inflammation proteinase-activated receptor distinct protease-activated receptor-2 immunoreactivity ischaemia–reperfusion microvascular damage protease-activated receptor-2 activation db/db+fsllry–nh2 article basic research protease-activated receptor-2 involvement related subjects alter ach-induced vasodilation db/db mice treated db/db mice null tnf-α induced shedding ikk-beta pathway contributes db/db mice compared nadph oxidase-derived overproduction myocardial ischemia-reperfusion injury par2 antagonist fsllry–nh2 coronary arteriolar dysfunction full article pdf endothelium-dependent vasodilation proteinase-activated receptor 2 protease-activated receptor-2 privacy choices/manage cookies tnf-alpha contributes endothelium-dependent acetylcholine coronary microembolization induced proteinase-activated receptors proteinase-activated-receptors 2 flow-mediated vasodilation protease-activated receptors myocardial ischemia/reperfusion beta-cell function cerebral artery vasodilatation db/db mice human coronary artery ischemia/reperfusion injury human endothelial cells article park increased vascular permeability vascular endothelial cells reperfusion salvages myocardium european economic area activator dh404 protects vivo lung function

Questions {❓}

Cocks TM, Moffatt JD (2000) Protease-activated receptors: sentries for inflammation?

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         headline:Effect of PAR2 in regulating TNF-α and NAD(P)H oxidase in coronary arterioles in type 2 diabetic mice
         description:Protease-activated receptor-2 (PAR2) is expressed in endothelial cells and mediates endothelium-dependent vasodilation. We hypothesized that PAR2 regulates tumor necrosis factor-alpha (TNF-α)-induced coronary arteriolar dysfunction in type 2 diabetic (db/db) mice. To test this, coronary arterioles from WT control, db/db, db/db mice treated with PAR2 antagonist FSLLRY–NH2 (db/db+FSLLRY–NH2) and db/db mice null for TNF (dbTNF−/dbTNF−) were isolated and pressurized (60 cmH2O) without flow. Although vasodilation to the endothelium-independent vasodilator sodium nitroprusside (SNP) was not different among WT, db/db, db/db+FSLLRY–NH2 and dbTNF−/dbTNF−, endothelium-dependent acetylcholine (ACh)- and flow-mediated vasodilation were impaired in db/db mice but were enhanced in dbTNF−/dbTNF− mice and db/db mice treated with PAR2 antagonist. NOS inhibitor N G-nitro-l-arginine-methyl ester (l-NAME) significantly reduced ACh-induced dilation in WT, dbTNF−/dbTNF− and db/db+FSLLRY–NH2, but did not alter the vasodilation in db/db mice. In contrast, cyclooxygenase (COX) inhibitor indomethacin (Indo) did not alter ACh-induced vasodilation in these four groups of mice. PAR2-activating peptide (PAR2-AP, 2-Furoyl-LIGRLO-am)-induced dilation was higher in db/db mice than that in WT, dbTNF−/dbTNF− and db/db mice treated with PAR2 antagonist. These effects were abolished by denudation, or in the presence of l-NAME or Indo. Protein expressions of TNF-α, PAR2, gp91phox and p47phox in the heart and isolated coronary arterioles were higher in db/db mice compared to WT mice. Administration of PAR2 antagonist to db/db mice reduced protein expression of TNF-α, gp91phox and PAR2. Protein expression of gp91phox and p47phox was lower in dbTNF−/dbTNF− compared to db/db mice. These results indicate that PAR2 plays a pivotal role in endothelial dysfunction in type 2 diabetes by up-regulating the expression/production of TNF-α and activating NAD(P)H oxidase subunit p47phox.
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