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

Min Jeong Kim, Jin Sook Kwon, Suk Hyo Suh, Jae Kyung Suh, Jaehoon Jung, Si Nae Lee, Young Hwa Kim, Myeong Chan Cho, Goo Taeg Oh, Kyunglim Lee

Research output: Contribution to journalArticlepeer-review

44 Scopus citations

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.

Original languageEnglish
Pages (from-to)151-159
Number of pages9
JournalJournal of Molecular and Cellular Cardiology
Volume44
Issue number1
DOIs
StatePublished - Jan 2008

Keywords

  • Calcium
  • Hypertension
  • K-ATPase
  • Na
  • Translationally controlled tumor protein (TCTP)
  • Vascular contractility

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