Milano C A, Dolber P C, Rockman H A, Bond R A, Venable M E, Allen L F, Lefkowitz R J
Department of Surgery, Duke University Medical Center, Durham, NC 27710.
Proc Natl Acad Sci U S A. 1994 Oct 11;91(21):10109-13. doi: 10.1073/pnas.91.21.10109.
Transgenic mice were generated by using the alpha-myosin heavy chain promoter coupled to the coding sequence of a constitutively active mutant alpha 1B-adrenergic receptor (AR). These transgenic animals demonstrated cardiac-specific expression of this alpha 1-AR with resultant activation of phospholipase C as shown by increased myocardial diacylglycerol content. A phenotype consistent with cardiac hypertrophy developed in adult transgenic mice with increased heart/body weight ratios, myocyte cross-sectional areas, and ventricular atrial natriuretic factor mRNA levels relative to nontransgenic controls. These transgenic animals may provide insight into the biochemical triggers that induce hypertrophy in cardiac disease and serve as a convenient experimental model for studies of this condition.
通过使用与组成型活性突变α1B - 肾上腺素能受体(AR)编码序列偶联的α - 肌球蛋白重链启动子来产生转基因小鼠。这些转基因动物表现出该α1 - AR的心脏特异性表达,如心肌二酰甘油含量增加所示,导致磷脂酶C激活。成年转基因小鼠出现与心脏肥大一致的表型,相对于非转基因对照,其心脏/体重比、心肌细胞横截面积和心室心房利钠因子mRNA水平增加。这些转基因动物可能有助于深入了解诱发心脏病中肥大的生化触发因素,并作为研究这种病症的便捷实验模型。