Endothelin-1 Induces Contraction via a Syk-Mediated p38 Mitogen-Activated Protein Kinase Pathway in Rat Aortic Smooth Muscle

Lee, Hwan Myung; Won, Kyung‐Jong; Kim, Junghwan; Park, Hyojun; Kim, Hyo Jin; Roh, Hui Yul; Lee, So Hee; Lee, Chang-Kwon; Kim, Bokyung

doi:10.1254/jphs.fp0070039

Cited by 31 publications

(28 citation statements)

References 35 publications

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“…In many smooth muscles, p38 MAPK activation is linked to contraction (10,29,34,36,56), and in vascular tissues and gastrointestinal smooth muscle cells, Hsp27 phosphorylation is important for sustained contraction (32,40). Although in rat aorta smooth muscle cells, the inhibition of p38 MAPK and Hsp27 showed a significant reduction in contraction to ANG II but not NE (34).…”

Section: Discussionmentioning

confidence: 99%

Regulation of contractility by Hsp27 and Hic-5 in rat mesenteric small arteries

Srinivasan¹,

Forman²,

Quinlan³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

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regulation of small artery contractility by vasoconstrictors is important for vascular function, and actin cytoskeleton remodeling is required for contraction. p38 MAPK and tyrosine kinases are implicated in actin polymerization and contraction through heat shock protein 27 (Hsp27) and the cytoskeletal protein paxillin, respectively. We evaluated the roles of downstream targets of p38 MAPK and tyrosine kinases in cytoskeletal reorganization and contraction and whether the two signaling pathways regulate contraction independent of each other. We identified the expression of the paxillin homologue hydrogen peroxide-inducible clone-5 (Hic-5) and showed its activation by norepinephrine (NE) in a Src-dependent manner. Furthermore, we demonstrated a NE-induced interaction of proline-rich tyrosine kinase-2 (PYK2) but not Src or p125 focal adhesion kinase with Hic-5. This interaction was Src dependent, suggesting that Hic-5 was a substrate for PYK2 downstream from Src. The activation of Hic-5 induced its relocalization to the cytosol. The parallel activation of Hsp27 by NE was p38 MAPK dependent and led to its dissociation from actin filaments and translocation from membrane to cytosol and increased actin polymerization. Both Hsp27 and Hic-5 activation resulted in their association within the same time frame as NEinduced contraction, and the inhibition of either p38 MAPK or Src inhibited the interaction between Hsp27 and Hic-5 and the contractile response. Furthermore, combined p38 MAPK and Src inhibition had no greater effect on contraction than individual inhibition, suggesting that the two pathways act through a common mechanism. These data show that NE-induced activation and the association of Hsp27 and Hic-5 are required for the reorganization of the actin cytoskeleton and force development in small arteries.

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Section: Discussionmentioning

confidence: 99%

Regulation of contractility by Hsp27 and Hic-5 in rat mesenteric small arteries

Srinivasan¹,

Forman²,

Quinlan³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

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“…Some drugs are also known to contract smooth muscle 2,3) . Many previous studies, including our own, have reported on signal transduction mechanisms and smooth muscle contractions [4][5][6][7][8][9][10][11][12][13][14] . In spite of the importance of the smooth muscle in the fields of cardiovascular physiotherapy, obstetrics, and clinical methods, there is still a need for more research [15][16][17] .…”

Section: Introductionmentioning

confidence: 89%

“…Syk is also found in bronchial smooth muscle and has attracted attention because of its role in hypertension and the emigration of smooth muscle related to arteriosclerosis (Fig. 11-B) 11,91,92) . The N-terminal of Syk protein has two Src-homology 2 (SH2) domains.…”

Section: ) Syk Protein Tyrosine Kinase (Syk) Involvement In Smooth Mmentioning

confidence: 99%

“…Recently, the protein kinase C (PKC) pathway, the mitogen-activated protein kinase (MAPK) pathway, the rho-associated coiled coil-forming protein kinase (ROCK) pathway, and the phosphatidylinositol 3-kinase (PI3 K) pathway have also been reported to be involved in smooth muscle contractions 18,19) . The activation of caldesmon (CaD) 8,20,21) and heat shock protein 27 (HSP27) are now believed to occur in smooth muscle contractions as well 11,22) . The aim of this review is to collate the body of knowledge on smooth muscle contractions and the pathways involved in order to prepare a basic reference for cardiovascular physiotherapy.…”

Section: Introductionmentioning

confidence: 99%

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A Review of Signal Transduction in Mechanisms of Smooth Muscle Contraction and Its Relevance for Specialized Physical Therapy

Kim

Lee

et al. 2013

J Phys Ther Sci

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Abstract.[Purpose] An understanding of smooth muscle contraction is important in the study of specialized physical therapy. In this paper, we summarize the contraction mechanisms of smooth muscle and suggest their applications in physical therapy. [Method] This review focuses on the signaling pathways that control smooth muscle contraction and its mechanisms. We include results reported by our laboratory in a wider literature review. [Results] Our results and the literature show that various mechanisms of smooth muscle contraction exist. [Conclusions] In this review article, we carefully discuss the signal transduction in smooth muscle contraction based on our studies and with reference to physical therapy.

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“…In addition, elevated ET-1 levels lead to NADPH oxidase activation and superoxide formation via ET A receptors, resulting in excessive ROS production and endothelial dysfunction [14]. Other studies have demonstrated that the kinases (p38 MAPK, ERK1/2) and NF-κB signaling pathways take part in the regulation of ET-1 in response to a variety of stimuli [15].…”

Section: Introductionmentioning

confidence: 99%