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• W2019574076 abstract "This study was designed to evaluate the signaling pathways coupling adenosine A₁ receptors and extracellular signal-regulated kinase (ERK) 1 and 2 in human trabecular meshwork (HTM) cells. Studies were conducted using cultures of primary HTM cells and the HTM-3 cell line. Activation of ERK1/2, location of protein kinase C (PKC) isoforms, and matrix metalloproteinase (MMP) secretion were determined by Western blotting. In primary HTM cells and the HTM-3 cell line, administration of the A₁ agonist <i>N</i>⁶-cyclohexyladenosine (CHA) produced a concentration-dependent increase in ERK1/2 activation. This CHA-induced ERK activation was blocked by pretreatment with the A₁ receptor antagonist 8-cyclopentyl-1,3-dimethylxanthine or pertussis toxin. Transfection with dominant negative N17 Ras produced only a small (31%) decline in CHA-induced ERK activation, and the response was not altered by pretreatment with the Src tyrosine kinase inhibitor, PP2 [3-(4-chlorophenyl)1-(1,1-dimethylethyl)-1<i>H</i>-pyrazolo[3,4-D] pyrimidin-4-amine], the phosphoinositide kinase-3 inhibitor, LY-294002 [2-(4-morpholinyl)-8-phenyl-4<i>H</i>-1-benzopyran-4-one], or the A₃ receptor antagonist, MRS-1191 [3-ethyl-5-benzyl-2-methyl-4-phenylethynyl-6-phenyl-1,4-(±)-dihydropyridine-3,5-dicarboxylate]. Administration of CHA also induced the translocation of PKCα from the cytosol to the membrane, and pretreatment with the phospholipase C (PLC) inhibitor, U73122 [1-[6-[[(17β)-3-methoxyestra-1,3,5(10)-trien-17-yl]amino]-hexyl]-1<i>H</i>-pyrrole-2,5-dione], blocked ERK1/2 activation induced by CHA. Transfection of short interfering RNA targeting PKCα blocked the CHA-induced ERK1/2 activation and the secretion of MMP-2. These results confirm the existence of functional adenosine A₁ receptors in the trabecular meshwork cells. These receptors are coupled to the activation of ERK1/2 through G_i/o proteins and dependent upon the upstream activation of PLC and PKCα. These studies provide evidence that adenosine A₁ receptor agonists increase outflow facility through sequential activation of G_i/o > PLC > PKCα > c-Raf > mitogen-activated protein kinase kinase > ERK1/2, leading to secretion of MMP-2." @default.
• W2019574076 created "2016-06-24" @default.
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• W2019574076 date "2006-10-02" @default.
• W2019574076 modified "2023-10-18" @default.
• W2019574076 title "Mechanisms Linking Adenosine A₁ Receptors and Extracellular Signal-Regulated Kinase 1/2 Activation in Human Trabecular Meshwork Cells" @default.
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• W2019574076 doi "https://doi.org/10.1124/jpet.106.110981" @default.
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