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Transgenic overexpression of translationally controlled tumor protein induces systemic hypertension via repression of Na+,K+-ATPase

Title
Transgenic overexpression of translationally controlled tumor protein induces systemic hypertension via repression of Na+,K+-ATPase
Authors
Kim M.-J.Kwon J.-S.Suh S.H.Suh J.-K.Jung J.Lee S.-N.Kim Y.-H.Cho M.-C.Oh G.T.Lee K.
Ewha Authors
이경림서석효오구택
SCOPUS Author ID
이경림scopus; 서석효scopus; 오구택scopus
Issue Date
2008
Journal Title
Journal of Molecular and Cellular Cardiology
ISSN
0022-2828JCR Link
Citation
vol. 44, no. 1, pp. 151 - 159
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
Inhibition of Na+,K+-ATPase has been implicated in the pathogenesis of hypertension via its effect on smooth muscle reactivity and myocardial contractility. We recently demonstrated that translationally controlled tumor protein (TCTP) interacts with the 3rd cytoplasmic domain of Na+,K+-ATPase α1-subunit and acts as its cytoplasmic repressor. Therefore, we hypothesized that repression of Na+,K+-ATPase by overexpressed TCTP might underlie the development of hypertension. In the present study, we confirmed that transgenic mice overexpressing TCTP developed systemic arterial hypertension at about 6 weeks after birth. Vascular smooth muscle of TCTP-overexpressing transgenic mice also displayed augmented contractile response to vasoconstrictors and attenuated relaxation response to vasodilators. These responses seem to be caused by reduced Na+,K+-ATPase activity and increased intracellular calcium, suggesting that inhibition of Na+,K+-ATPase by overexpression of TCTP is involved in the pathogenesis of hypertension. This study provides a new link between alteration of sodium pump activity and hypertension in vivo, and suggests that TCTP might be a therapeutic target for the treatment of hypertension. © 2007 Elsevier Inc. All rights reserved.
DOI
10.1016/j.yjmcc.2007.09.017
Appears in Collections:
약학대학 > 약학과 > Journal papers
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