Reactive Oxygen Species Mediate ET-1-Induced Activation of ERK1/2 Signaling in Cultured Feline Esophageal Smooth Muscle Cells

Song, Hyun-Ju; Kim, Ji-Soo; Lee, Myong-Jae; Nam, Yun-Sung; Sohn, Uy-Dong

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자료유형: 학술저널

저자정보: Song, Hyun-Ju (Department of Pharmacology, College of Pharmacy, Chung Ang University) Kim, Ji-Soo (Department of Pharmacology, College of Pharmacy, Chung Ang University) Lee, Myong-Jae (Department of Pharmacology, College of Pharmacy, Chung Ang University) Nam, Yun-Sung (Department of Pharmacology, College of Pharmacy, Chung Ang University) Sohn, Uy-Dong (Department of Pharmacology, College of Pharmacy, Chung Ang University)

저널정보: 대한약학회 Archives of pharmacal research : a publication of the Pharmaceutical Society of Korea Archives of pharmacal research : a publication of the Pharmaceutical Society of Korea 제30권 제9호

발행연도: 2007.1

수록면: 1,080 - 1,087 (8page)

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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.

#ERK1/2 #ET-1 #Esophageal Smooth Muscle Cells #lROS

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