Skip Navigation

Cardiovascular Research 2003 58(1):149-155; doi:10.1016/S0008-6363(02)00842-8
© 2003 by European Society of Cardiology
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Schäfer, C.
Right arrow Articles by Piper, H.M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Schäfer, C.
Right arrow Articles by Piper, H.M.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 2003, European Society of Cardiology

Inhibition of contractile activation reduces reoxygenation-induced endothelial gap formation

C. Schäfer, S. Walther, M. Schäfer, L. Dieterich, S. Kasseckert, Y. Abdallah and H.M. Piper*

Institute of Physiology, Justus-Liebig-University Giessen, Aulweg 129, D-35392 Giessen, Germany

* Corresponding author. Tel.: +49-641-99-47241; fax: +49-641-99-47239. michael.piper{at}physiologie.med.uni-giessen.de

Objective: Barrier function of coronary endothelium becomes disturbed by ischemia–reperfusion. We investigated the mechanism of reperfusion-induced endothelial gap formation in monolayers of cultured endothelial cells (CEC) of the rat, exposed to simulated ischemia (40 min anoxia, pHo 6.4) and reperfusion (30 min reoxygenation, pHo 7.4). Methods: Cytosolic Ca2+ (fura-2) and intercellular gap formation (planimetrical analysis) were determined. Reoxygenation conditions were varied: (a) continuing perfusion at pHo 6.4, (b) with or without glucose (2.5 mM), (c) in presence of NaCN (2 mM), (d) with Ca2+ (10 mM) or BAPTA/AM (25 µM), (e) in the presence of myosin light chain kinase inhibitors ML-7 (5 µM) or wortmannin (1 µM). Results: During anoxia, CEC developed cytosolic Ca2+ overload which was not reversed during 30 min reoxygenation. Intercellular gap formation started during anoxia, but was increased during reoxygenation. Reoxygenation-related gap formation was largest in presence of glucose, lower when glucose was withdrawn or NaCN was added. Presence of ML-7 or wortmannin also reduced gap formation during reoxygenation. Conclusions: Reoxygenation induces gap formation. This is dependent on (i) Ca2+ overload during reoxygenation, (ii) energy production and (iii) activation of myosin light chain kinase. Together these results indicate that activation of the endothelial contractile machinery is the underlying cause.

KEYWORDS Calcium (cellular); Contractile apparatus; Endothelial function; Ischemia; Reperfusion

* The review process and the Editorial decision was the responsibility of the previous Editorial team.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Cardiovasc ResHome page
S. A. Kasseckert, C. Schafer, A. Kluger, D. Gligorievski, J. Tillmann, K.-D. Schluter, T. Noll, H. Sauer, H. M. Piper, and Y. Abdallah
Stimulation of cGMP signalling protects coronary endothelium against reperfusion-induced intercellular gap formation
Cardiovasc Res, July 15, 2009; 83(2): 381 - 387.
[Abstract] [Full Text] [PDF]

Home page
 Cardiovasc ResHome page
S. C. Peters and H. M. Piper
Reoxygenation-induced Ca2+ rise is mediated via Ca2+ influx and Ca2+ release from the endoplasmic reticulum in cardiac endothelial cells
Cardiovasc Res, January 1, 2007; 73(1): 164 - 171.
[Abstract] [Full Text] [PDF]

Home page
 Cardiovasc ResHome page
D. Gunduz, S. A. Kasseckert, F. V. Hartel, M. Aslam, Y. Abdallah, M. Schafer, H. M. Piper, T. Noll, and C. Schafer
Accumulation of extracellular ATP protects against acute reperfusion injury in rat heart endothelial cells
Cardiovasc Res, September 1, 2006; 71(4): 764 - 773.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.