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Reactive oxygen species mediate ET-1-induced activation of ERK1/2 signaling in cultured feline esophageal smooth muscle cells.

Reactive oxygen species mediate ET-1-induced activation of ERK1/2 signaling in cultured feline esophageal smooth muscle cells. Research Abstract Details 

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  • Reactive oxygen species mediate ET-1-induced activation of ERK1/2 signaling in cultured feline esophageal smooth muscle cells. Abstract Text:

    hyun ju songHyun Ju Song,ji soo kimJi Soo Kim,myong jae leeMyong Jae Lee,yoon sung namYoon Sung Nam,uy dong sohnUy Dong Sohn,

    Reactive oxygen species (ROS) have been shown to play a critical role in propagating the signals of several growth factors, peptide hormones, and cytokines, such as epidermal growth factor, insulin, and interleukin-1. We investigated a possible role for ROS generation in mediating the action of ET-1 on activation of ERK1/2 in cultured feline esophageal smooth muscle cells (ESMC). Confluent layers of ESMC were stimulated by 10nM ET-1; activation of ERK was examined by western blot analysis with phospho-specific antibodies of ERKs. ET-1 induced ERK1/2 phosphorylation in a dose- and time- dependent manner. ERK1/2 activation by ET-1 reached the maximal levels at 5min showing slight activation up to 20min, and then slowly declined. It was confirmed that the activation of ERK1/2 was reduced by MEK inhibitor PD98059. We observed the dose-dependent inhibitory effect of diphenyleneiodonium (DPI), an inhibitor of reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase on the ET-1-enhanced ERK1/2 phosphorylation in ESMC. Pretreatment of ESMC with N-acetylcysteine, a ROS scavenger, also attenuated the ET-1-induced ERK1/2 activation. In addition, DPI significantly inhibited the ET-1- induced ROS production when ROS was measured as a function of DCF fluorescence. The results suggest that ROS might be critical mediators of the ET-1-induced ERK1/2 signaling events in ESMC.

    Reactive oxygen species mediate ET-1-induced activation of ERK1/2 signaling in cultured feline esophageal smooth muscle cells. Publishing Authors By Initials

    hj songHJ Song,js kimJS Kim,mj leeMJ Lee,ys namYS Nam,ud sohnUD Sohn,

    For similar inorganic chemicals: free radicals: reactive oxygen species research abstracts see: inorganic chemicals: free radicals: reactive oxygen species research

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    Reactive oxygen species mediate ET-1-induced activation of ERK1/2 signaling in cultured feline esophageal smooth muscle cells. Journal Published:

    PUBLICATION TYPE: Journal Article

    Journal: Archives of pharmacal research

    VOLUME: 30

    Page Numbers: 1080-7

    Journal Abbreviation: Arch. Pharm. Res.

    ISSN: 0253-6269

    DAY: 20

    MONTH: Sep

    YEAR: 2007

    Reactive oxygen species mediate ET-1-induced activation of ERK1/2 signaling in cultured feline esophageal smooth muscle cells. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 8000036

    Reactive oxygen species mediate ET-1-induced activation of ERK1/2 signaling in cultured feline esophageal smooth muscle cells. Keywords Mesh Terms:

    KEYWORDS: Reactive Oxygen Species

    MESH TERMS: metabolism

    Chemical & Substance for Abstract: Reactive oxygen species mediate ET-1-induced activation of ERK1/2 signaling in cultured feline esophageal smooth muscle cells. Information

    Substance Name: Mitogen-Activated Protein Kinase 3

    Registry Number: EC 2.7.1.37

    Grant and Affiliation Information for Reactive oxygen species mediate ET-1-induced activation of ERK1/2 signaling in cultured feline esophageal smooth muscle cells.

    AFFILIATION: Department of Pharmacology, College of Pharmacy, Chung Ang University, Seoul 156-756, Korea.

    Country: Korea (South)

    Korea (South) Research PublicationKorea (South) Research Publication

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    MEDLINETA: Arch Pharm Res

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