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

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

doi:10.1254/jphs.FP0070039

Full Papers

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

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

Author information

Hwan Myung Lee
Departments of Physiology, College of Medicine, Konkuk University, Korea
Kyung-Jong Won
Departments of Physiology, College of Medicine, Konkuk University, Korea
Junghwan Kim
Department of Physical Therapy, College of Natural Science, Yongin University, Korea
Hyo-Jun Park
Departments of Physiology, College of Medicine, Konkuk University, Korea
Hyo Jin Kim
Departments of Physiology, College of Medicine, Konkuk University, Korea
Hui Yul Roh
Departments of Physiology, College of Medicine, Konkuk University, Korea
So Hee Lee
Departments of Physiology, College of Medicine, Konkuk University, Korea
Chang-Kwon Lee
Departments of Physiology, College of Medicine, Konkuk University, Korea
Bokyung Kim
Departments of Physiology, College of Medicine, Konkuk University, Korea

Keywords: contraction, spleen tyrosine kinase (Syk), rat aortic smooth muscle cell (RASMC), endothelin-1, p38 mitogen-activated protein kinase (MAPK)

JOURNAL FREE ACCESS

2007 Volume 103 Issue 4 Pages 427-433

DOI https://doi.org/10.1254/jphs.FP0070039

View "Advance Publication" version (March 31, 2007).

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Abstract

Although spleen tyrosine kinase (Syk) has crucial roles in various cells, its function on vascular smooth muscle contraction has not been determined. In the present study, we performed experiments to determine if Syk contributes to the endothelin-1 (ET-1)-mediated contraction in rat aortic smooth muscle. ET-1-induced contraction of aortic strips was inhibited by piceatannol, PD98059, and SB203580, inhibitors of Syk, extracellular signal-regulated kinase 1/2 (ERK1/2), and p38 mitogen-activated protein kinase (MAPK), respectively. Piceatannol also attenuated high K⁺-induced contraction. ET-1 dose-dependently enhanced the activity of Syk and this was inhibited by piceatannol in both rat aortic strip and rat aortic smooth muscle cells. The phosphorylation of p38 MAPK and heat shock protein 27 (HSP27), but not that of ERK1/2, in response to ET-1 was inhibited by both piceatannol and SB203580. These results suggest that Syk may play an important role in the regulation of aortic smooth muscle contraction induced by ET-1, which may be mediated by the p38 MAPK/HSP27 signaling pathway.

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