Cyclic stretch downregulates arterial vascular connexin43 protein expression: an ex vivo study |
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Authors: | Yong He Sanjeev G Shroff |
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Institution: | (1) Department of Biomedical Engineering, University of Wisconsin, Madison, WI 53706-1609, USA;(2) Department of Biomedical Engineering, University of Wisconsin-Madison, 2146 Engineering Centers Building, 1550 Engineering Drive, Madison, WI 53706-1609, USA; |
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Abstract: | Vascular cells may communicate through gap junctions that are formed by connexin (Cx) proteins. We investigated differential
regulation of arterial gap junctions by steady and cyclic stretch and the underlying mechanotransduction pathways. Ex vivo
culture of rabbit thoracic aortas was used to investigate regulation of Cx43 by cyclic stretch. After culturing for 6 or 24
h, Cx43 protein levels were quantified using Western blot. Cultures under a pulsatile pressure (mean 80 mmHg, pulse 30 mmHg)
decreased Cx43 protein at both 6 and 24 h as compared with cultures under a steady pressure (80 mmHg). The regulation of Cx43
protein was mediated by pulsatile pressure-induced cyclic stretch, not by cyclic stress. Protein levels of active and total
Src were also decreased by cyclic stretch at 24 h. The Src- specific inhibitor PP1 in steady culture only or in both steady
and pulsatile culture conditions eliminated the difference in Cx43 protein levels between the two culture conditions. Addition
of reactive oxygen species inhibitor apocynin to the pulsatile culture abolished the differences in Src and Cx43 protein levels
between the two cultures. Thus, Src and reactive oxygen species appear to play a role in cyclic stretch-mediated regulation
of Cx43 protein. These results are likely to have important implications in cardiovascular physiology and pathophysiology
under conditions wherein significant alterations in the level of cyclic stretch are present. |
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