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This Article Full Text Full Text (PDF) All Versions of this Article: 577/3/1033    most recent jphysiol.2006.118828v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Babu, G. J. Articles by Periasamy, M. Search for Related Content PubMed PubMed Citation Articles by Babu, G. J. Articles by Periasamy, M. Related Collections Integrative

¹ Department of Physiology and Cell Biology, The Ohio State University, College of Medicine and Public Health, 304 Hamilton Hall, 1645 Neil Ave, Columbus, OH 43210, USA
² Department of Obstetrics and Gynecology, University of Vermont College of Medicine, Given C-217A, 89 Beaumont Dr, Burlington, VT 05405, USA
³ Department of Physiology and Biophysics, Case Western Reserve University, 10900 Euclid Avenue, Cleveland, OH 44106, USA
⁴ Department of Molecular Medicine and Pathophysiology, Osaka Medical Center for Cancer and Cardiovascular Diseases, Osaka University, Osaka 537-8511, Japan

The functional significance of smooth muscle-specific h1-calponin up-regulation in the smooth muscle contractility of SM-B null mice was studied by generating double knockout mice lacking both h1-calponin and SM-B myosin. The double knockout mice appear healthy, reproduce well and do not show any smooth muscle pathology. Loss of h1-calponin in the SM-B null mice bladder resulted in increased maximal shortening velocity (V_max) and steady-state force generation. The force dilatation pressure, which was decreased in the SM-B null mesenteric vessels, was restored to wild-type levels in the double knockout vessels. In contrast, the half-time to maximal constriction was significantly increased in the double knockout vessels similar to that of SM-B null mice and indicating decreased shortening velocity in the double knockout vessels. Biochemical analyses showed that there is a significant reduction in smooth muscle -actin levels, whereas h-caldesmon levels are increased in the double knockout bladder and mesenteric vessels, suggesting that these changes may also partly contribute to the altered contractile function. Taken together, our studies suggest that up-regulation of h1-calponin in the SM-B null mice may be necessary to maintain a reduced level of cross-bridge cycling over time in the absence of SM-B myosin and play an important role in regulating the smooth muscle contraction.

(Received 7 August 2006; accepted after revision 7 September 2006; first published online 14 September 2006)
Corresponding author G. J. Babu: Department of Physiology and Cell Biology, The Ohio State University College of Medicine and Public Health, 304 Hamilton Hall, 1645 Neil Ave, Columbus, OH 43210, USA.  Email: babu.10{at}osu.edu