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Am J Physiol Heart Circ Physiol (December 22, 2005). doi:10.1152/ajpheart.00772.2004
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Submitted on July 30, 2004
Accepted on December 14, 2005

Calpains - a physiological regulator of the endothelial barrier?

Vera Gonscherowski1, Bernhard F Becker1*, Luis Moroder2, Elena Motrescu3, Shirley Gil-Parrado4, Torsten Gloe1, Matthias Keller1, and Stefan Zahler1

1 Physiology, University of Munich, Munich, Germany
2 Biochemistry, Max-Plank-Institute, Martinsried, Germany
3 Medical Elecrtonics, Technical University, Munich, Germany
4 Clinical Chemistry and Clinical Biochemistry, University of Munich, Munich, Germany

* To whom correspondence should be addressed. E-mail: B.F.Becker{at}lrz.uni-muenchen.de.

The intracellular protease calpain, abundant in endothelial cells (EC), is assumed to be inactive under physiological conditions but may account for Ca++-linked pathophysiological events. However, non-stimulated EC contained autolysed, activated calpain. Adding 12-48µM calpain inhibitor I (CI) or 0.5-1µM of the novel, membrane permeable conjugate of calpastatin peptide-penetratin (CPP) caused rapid rounding and retraction of cultured EC (phase contrast, capacitance), and translocation of Syk, Rac and Rho to the membrane, signifying activation upon inhibition of calpain. Isolated hearts (guinea pig) perfused with 12 µM CI or 0.5 µM CPP developed coronary leak. We conclude that calpain is constitutively active in EC and regulates vascular permeability by governing cell-cell attachment.




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