AJP - Heart Watch the video to learn how APS reaches out to developing nations.
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Heart Circ Physiol 282: H2124-H2133, 2002. First published March 7, 2002; doi:10.1152/ajpheart.01028.2001
0363-6135/02 $5.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
282/6/H2124    most recent
01028.2001v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Web of Science (24)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Li, H.
Right arrow Articles by Goligorsky, M. S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Li, H.
Right arrow Articles by Goligorsky, M. S.
Vol. 282, Issue 6, H2124-H2133, June 2002

Paradoxical overexpression and translocation of connexin43 in homocysteine-treated endothelial cells

Hong Li1, Sergey Brodsky1, Sindu Kumari2, Virginijus Valiunas2, Peter Brink2, Jun-Ichi Kaide3, Alberto Nasjletti3, and Michael S. Goligorsky1,2

Departments of 1 Medicine and 2 Physiology and Biophysics, State University of New York, Stony Brook 11794; and 3 Department of Pharmacology, New York Medical College, Valhalla, New York 10595

Hyperhomocysteinemia is an established cause of defective vasorelaxation. Gene expression screening of human umbilical vein endothelial cells (HUVEC) treated with homocysteine (Hcy) revealed that connexin43 (Cx43) was upregulated. Expression of Cx43 was increased more than twofold in Hcy-treated HUVEC. Gap junctional communication (Lucifer yellow and whole cell patch clamp) was not enhanced in Hcy-treated HUVEC. HUVEC expressing chimeric Cx43-green fluorescent protein exhibited it at cell-cell contacts in control but showed redistribution to the intracellular compartment(s) in Hcy-treated cells. Confocal microscopy of HUVEC stained with anti-Cx43, mitochondrial, and endoplasmic reticulum fluorescent markers showed the localization of Cx43 to the plasma membrane of control cells and its colocalization with the mitochondrial marker in Hcy-treated HUVEC. Studies of isolated mitochondria confirmed overexpression of Cx43 in the mitochondria of Hcy-treated HUVEC. Microdissected renal interlobar arteries, which normally exhibit endothelium-derived hyperpolarizing factor-induced vasorelaxation, showed reduced nitric oxide synthase- and cyclooxygenase-independent vasorelaxation to acetylcholine after pretreatment with Hcy. In summary, Hcy-induced upregulation of Cx43 transcript and protein expression are associated with unaltered intercellular communication, redistribution of Cx43 in HUVEC, and reduced nitric oxide- and prostanoid-independent vascular responses to acetylcholine in Hcy-treated arteries.

gene microarray; mitochondria; endothelium-derived hyperpolarizing factor


This article has been cited by other articles:


Home page
 DMMHome page
H. Y. Stevens, B. Melchior, K. S. Bell, S. Yun, J.-C. Yeh, and J. A. Frangos
PECAM-1 is a critical mediator of atherosclerosis
Dis. Model. Mech., September 1, 2008; 1(2-3): 175 - 181.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
M. J. Crabtree, C. L. Smith, G. Lam, M. S. Goligorsky, and S. S. Gross
Ratio of 5,6,7,8-tetrahydrobiopterin to 7,8-dihydrobiopterin in endothelial cells determines glucose-elicited changes in NO vs. superoxide production by eNOS
Am J Physiol Heart Circ Physiol, April 1, 2008; 294(4): H1530 - H1540.
[Abstract] [Full Text] [PDF]

Home page
 Cardiovasc ResHome page
M. Ruiz-Meana, A. Rodriguez-Sinovas, A. Cabestrero, K. Boengler, G. Heusch, and D. Garcia-Dorado
Mitochondrial connexin43 as a new player in the pathophysiology of myocardial ischaemia-reperfusion injury
Cardiovasc Res, January 15, 2008; 77(2): 325 - 333.
[Abstract] [Full Text] [PDF]

Home page
 J. Am. Soc. Nephrol.Home page
M. S. Goligorsky
Frontiers in Nephrology: Viewing the Kidney through the Heart Endothelial Dysfunction in Chronic Kidney Disease
J. Am. Soc. Nephrol., November 1, 2007; 18(11): 2833 - 2835.
[Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
V. Garg and K. Hu
Protein kinase C isoform-dependent modulation of ATP-sensitive K+ channels in mitochondrial inner membrane
Am J Physiol Heart Circ Physiol, July 1, 2007; 293(1): H322 - H332.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Renal Physiol.Home page
M. S. Goligorsky
Endothelial cell dysfunction: can't live with it, how to live without it
Am J Physiol Renal Physiol, May 1, 2005; 288(5): F871 - F880.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
S. V. Brodsky, F. Zhang, A. Nasjletti, and M. S. Goligorsky
Endothelium-derived microparticles impair endothelial function in vitro
Am J Physiol Heart Circ Physiol, May 1, 2004; 286(5): H1910 - H1915.
[Abstract] [Full Text] [PDF]

Home page
 Circ. Res.Home page
S. V. Brodsky, O. Gealekman, J. Chen, F. Zhang, N. Togashi, M. Crabtree, S. S. Gross, A. Nasjletti, and M. S. Goligorsky
Prevention and Reversal of Premature Endothelial Cell Senescence and Vasculopathy in Obesity-Induced Diabetes by Ebselen
Circ. Res., February 20, 2004; 94(3): 377 - 384.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online