Nonmuscle myosin II-B is required for normal development of the mouse heart

• DOI: 10.1073/pnas.94.23.12407
• Publication Date: 2002-07-26T14:31:44Z
• Authors: Antonella N. Tullio; Domenico Accili; Victor J. Ferrans; Zu-Xi Yu; Kazuyo Takeda; Alexander Grinberg; Heiner Westphal; Yvette A. Preston; Robert S. Adelstein
• Keywords: Cardiac myocyte

We used targeted gene disruption in mice to ablate nonmuscle myosin heavy chain B (NMHC-B), one of the two isoforms II present all vertebrate cells. Approximately 65% NMHC-B-/- embryos died prior birth, and those that were born suffered from congestive heart failure during first day. No abnormalities detected NMHC-B+/- mice. The absence NMHC-B resulted a significant increase transverse diameters cardiac myocytes 7.8 +/- 1.8 micron (right ventricle) 1.3 (left NMHC-B+/+ B+/- 14.7 1.1 13.8 2.3 micron, respectively, (in both cases, P < 0.001). size was seen as early embryonic day 12.5 (4.5 0.2 for vs. 7. 2 0.6 (P 0.01)). Six seven newborn analyzed by serial sectioning also showed structural defects, including ventricular septal defect, an aortic root either straddled defect or originated right ventricle, muscular obstruction outflow. Some hearts evidence up-regulation NMHC-A protein. These studies suggest II-B is required normal myocyte development its results defects resembling, part, common human congenital diseases, tetralogy Fallot double outlet ventricle.