These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Rottlerin activates AMPK possibly through LKB1 in vascular cells and tissues.
    Author: Kojima K, Motoshima H, Tsutsumi A, Igata M, Matsumura T, Kondo T, Kawashima J, Ichinose K, Furukawa N, Inukai K, Katayama S, Goldstein BJ, Nishikawa T, Tsuruzoe K, Araki E.
    Journal: Biochem Biophys Res Commun; 2008 Nov 14; 376(2):434-8. PubMed ID: 18789895.
    Abstract:
    AMP-activated protein kinase (AMPK) is a cellular energy sensor involved in multiple cell signaling pathways that has become an attractive therapeutic target for vascular diseases. It is not clear whether rottlerin, an inhibitor of protein kinase Cdelta, activates AMPK in vascular cells and tissues. In the present study, we have examined the effect of rottlerin on AMPK in vascular smooth muscle cells (VSMCs) and isolated rabbit aorta. Rottlerin reduced cellular ATP and activated AMPK in VSMCs and rabbit aorta; however, inhibition of PKCdelta by three different methods did not activate AMPK. Both VSMCs and rabbit aorta expressed the upstream AMPK kinase LKB1 protein, and rottlerin-induced AMPK activation was decreased in VSMCs by overexpression of dominant-negative LKB1, suggesting that LKB1 is involved in the upstream regulation of AMPK stimulated by rottlerin. These data suggest for the first time that LKB1 mediates rottlerin-induced activation of AMPK in vascular cells and tissues.
    [Abstract] [Full Text] [Related] [New Search]