Title : Activation of GABA-A receptor ameliorates homocysteine-induced MMP-9 activation by ERK pathway.

Pub. Date : 2009 Jul

PMID : 19308943






6 Functional Relationships(s)
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1 Activation of GABA-A receptor ameliorates homocysteine-induced MMP-9 activation by ERK pathway. Homocysteine mitogen-activated protein kinase 1 Homo sapiens
2 We hypothesized that Hcy causes cerebrovascular remodeling by increasing redox stress and MMP-9 activity via the extracellular signal-regulated kinase (ERK) signaling pathway and by inhibition of GABA-A receptors, thus behaving as an inhibitory neurotransmitter. Homocysteine mitogen-activated protein kinase 1 Homo sapiens
3 We hypothesized that Hcy causes cerebrovascular remodeling by increasing redox stress and MMP-9 activity via the extracellular signal-regulated kinase (ERK) signaling pathway and by inhibition of GABA-A receptors, thus behaving as an inhibitory neurotransmitter. Homocysteine mitogen-activated protein kinase 1 Homo sapiens
4 In parallel, Hcy caused phosphorylation of ERK and selectively decreased levels of tissue inhibitors of metalloproteinase-4 (TIMP-4). Homocysteine mitogen-activated protein kinase 1 Homo sapiens
5 Furthermore muscimol attenuated Hcy-induced MMP-9 via ERK signaling pathway. Homocysteine mitogen-activated protein kinase 1 Homo sapiens
6 These results suggest that Hcy competes with GABA-A receptors, inducing the oxidative stress transduction pathway and leading to ERK activation. Homocysteine mitogen-activated protein kinase 1 Homo sapiens