c-Jun N-terminal Kinase Contributes to Norepinephrine-Induced Contraction Through Phosphorylation of Caldesmon in Rat Aortic Smooth Muscle

c-Jun N-terminal Kinase Contributes to Norepinephrine-Induced Contraction Through Phosphorylation of Caldesmon in Rat Aortic Smooth Muscle

Abstract.: Vascular smooth muscle contraction is mediated by activation of extracellular signal-regulated kinase (ERK) 1/2, an isoform of mitogen-activated protein kinase (MAPK). However, the role of stress-activated protein kinase/c-Jun N-terminal kinase (JNK) in vascular smooth muscle contraction...

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Main Authors: Youn Ri Lee, Chang-Kwon Lee, Hyo-Jun Park, Hyojin Kim, Junghwan Kim, Jaeheung Kim, Keun Sang Lee, Yun Lyul Lee, Kyung Ok Min, Bokyung Kim
Format: Article
Language:English
Published: Elsevier 2006-01-01
Series:Journal of Pharmacological Sciences
Online Access:http://www.sciencedirect.com/science/article/pii/S1347861319345232
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spelling doaj-e48a08c02c7f4cf394f0e895d7912aad2020-11-25T02:31:28ZengElsevierJournal of Pharmacological Sciences1347-86132006-01-011002119125c-Jun N-terminal Kinase Contributes to Norepinephrine-Induced Contraction Through Phosphorylation of Caldesmon in Rat Aortic Smooth MuscleYoun Ri Lee0Chang-Kwon Lee1Hyo-Jun Park2Hyojin Kim3Junghwan Kim4Jaeheung Kim5Keun Sang Lee6Yun Lyul Lee7Kyung Ok Min8Bokyung Kim9Department of Physiology, College of Medicine, Institute of Biomedical Science and Technology, Konkuk University, Danwol-dong 322, Chungju, Choong-Buk 380-701, KoreaDepartment of Physiology, College of Medicine, Institute of Biomedical Science and Technology, Konkuk University, Danwol-dong 322, Chungju, Choong-Buk 380-701, KoreaDepartment of Physiology, College of Medicine, Institute of Biomedical Science and Technology, Konkuk University, Danwol-dong 322, Chungju, Choong-Buk 380-701, KoreaDepartment of Physiology, College of Medicine, Institute of Biomedical Science and Technology, Konkuk University, Danwol-dong 322, Chungju, Choong-Buk 380-701, KoreaDepartment of Physiology, College of Medicine, Institute of Biomedical Science and Technology, Konkuk University, Danwol-dong 322, Chungju, Choong-Buk 380-701, KoreaDepartment of Physiology, College of Medicine, Institute of Biomedical Science and Technology, Konkuk University, Danwol-dong 322, Chungju, Choong-Buk 380-701, KoreaDepartment of Physiology, College of Medicine, Institute of Biomedical Science and Technology, Konkuk University, Danwol-dong 322, Chungju, Choong-Buk 380-701, KoreaDepartment of Physiology, College of Medicine, Hallym University, Hallymdaehak-gil 39, Chunchon 200-702, KoreaDepartment of Physical Therapy, College of Natural Science, Yongin University, Yongin 449-714, KoreaDepartment of Physiology, College of Medicine, Institute of Biomedical Science and Technology, Konkuk University, Danwol-dong 322, Chungju, Choong-Buk 380-701, Korea; Corresponding author. bkkim2@kku.ac.krAbstract.: Vascular smooth muscle contraction is mediated by activation of extracellular signal-regulated kinase (ERK) 1/2, an isoform of mitogen-activated protein kinase (MAPK). However, the role of stress-activated protein kinase/c-Jun N-terminal kinase (JNK) in vascular smooth muscle contraction has not been defined. We investigated the role of JNK in the contractile response to norepinephrine (NE) in rat aortic smooth muscle. NE evoked contraction in a dose-dependent manner, and this effect was inhibited by the JNK inhibitor SP600125. NE increased the phosphorylation of JNK, which was greater in aortic smooth muscle from hypertensive rats than from normotensive rats. NE-induced JNK phosphorylation was significantly inhibited by SP600125 and the conventional-type PKC (cPKC) inhibitor Gö6976, but not by the Rho kinase inhibitor Y27632 or the phosphatidylinositol 3-kinase inhibitor LY294002. Thymeleatoxin, a selective activator of cPKC, increased JNK phosphorylation, which was inhibited by Gö6976. SP600125 attenuated the phosphorylation of caldesmon, an actin-binding protein whose phosphorylation is increased by NE. These results show that JNK contributes to NE-mediated contraction through phosphorylation of caldesmon in rat aortic smooth muscle, and that this effect is regulated by the PKC pathway, especially cPKC. Keywords:: c-Jun N-terminal kinase, mitogen-activated protein kinase, vascular smooth muscle contraction, caldesmon, hypertensionhttp://www.sciencedirect.com/science/article/pii/S1347861319345232
collection DOAJ
language English
format Article
sources DOAJ
author Youn Ri Lee
Chang-Kwon Lee
Hyo-Jun Park
Hyojin Kim
Junghwan Kim
Jaeheung Kim
Keun Sang Lee
Yun Lyul Lee
Kyung Ok Min
Bokyung Kim
spellingShingle Youn Ri Lee
Chang-Kwon Lee
Hyo-Jun Park
Hyojin Kim
Junghwan Kim
Jaeheung Kim
Keun Sang Lee
Yun Lyul Lee
Kyung Ok Min
Bokyung Kim
c-Jun N-terminal Kinase Contributes to Norepinephrine-Induced Contraction Through Phosphorylation of Caldesmon in Rat Aortic Smooth Muscle
Journal of Pharmacological Sciences
author_facet Youn Ri Lee
Chang-Kwon Lee
Hyo-Jun Park
Hyojin Kim
Junghwan Kim
Jaeheung Kim
Keun Sang Lee
Yun Lyul Lee
Kyung Ok Min
Bokyung Kim
author_sort Youn Ri Lee
title c-Jun N-terminal Kinase Contributes to Norepinephrine-Induced Contraction Through Phosphorylation of Caldesmon in Rat Aortic Smooth Muscle
title_short c-Jun N-terminal Kinase Contributes to Norepinephrine-Induced Contraction Through Phosphorylation of Caldesmon in Rat Aortic Smooth Muscle
title_full c-Jun N-terminal Kinase Contributes to Norepinephrine-Induced Contraction Through Phosphorylation of Caldesmon in Rat Aortic Smooth Muscle
title_fullStr c-Jun N-terminal Kinase Contributes to Norepinephrine-Induced Contraction Through Phosphorylation of Caldesmon in Rat Aortic Smooth Muscle
title_full_unstemmed c-Jun N-terminal Kinase Contributes to Norepinephrine-Induced Contraction Through Phosphorylation of Caldesmon in Rat Aortic Smooth Muscle
title_sort c-jun n-terminal kinase contributes to norepinephrine-induced contraction through phosphorylation of caldesmon in rat aortic smooth muscle
publisher Elsevier
series Journal of Pharmacological Sciences
issn 1347-8613
publishDate 2006-01-01
description Abstract.: Vascular smooth muscle contraction is mediated by activation of extracellular signal-regulated kinase (ERK) 1/2, an isoform of mitogen-activated protein kinase (MAPK). However, the role of stress-activated protein kinase/c-Jun N-terminal kinase (JNK) in vascular smooth muscle contraction has not been defined. We investigated the role of JNK in the contractile response to norepinephrine (NE) in rat aortic smooth muscle. NE evoked contraction in a dose-dependent manner, and this effect was inhibited by the JNK inhibitor SP600125. NE increased the phosphorylation of JNK, which was greater in aortic smooth muscle from hypertensive rats than from normotensive rats. NE-induced JNK phosphorylation was significantly inhibited by SP600125 and the conventional-type PKC (cPKC) inhibitor Gö6976, but not by the Rho kinase inhibitor Y27632 or the phosphatidylinositol 3-kinase inhibitor LY294002. Thymeleatoxin, a selective activator of cPKC, increased JNK phosphorylation, which was inhibited by Gö6976. SP600125 attenuated the phosphorylation of caldesmon, an actin-binding protein whose phosphorylation is increased by NE. These results show that JNK contributes to NE-mediated contraction through phosphorylation of caldesmon in rat aortic smooth muscle, and that this effect is regulated by the PKC pathway, especially cPKC. Keywords:: c-Jun N-terminal kinase, mitogen-activated protein kinase, vascular smooth muscle contraction, caldesmon, hypertension
url http://www.sciencedirect.com/science/article/pii/S1347861319345232
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