Re-expression of ACTA1 that encodes α-smooth muscle actin has been associated with cardiac hypertrophy in vitro and in vivo, in animal models and humans (43, 44).
The human ACTN3 gene encodes α-actinin-3, an actin-binding protein with a pivotal role in muscle structure and metabolism.
The human ACTN3 gene encodes α-actinin-3, an actin-binding protein with a structural role at the sarcomeric Z-line in glycolytic (type II, fast-twitch) muscle fibers, and plays an increasingly evident role in the regulation of muscle metabolism [2].
As seen, in figure 6A and 6B, postnatal loss of Dicer in SMC of adult mice also result in reduced expression of contractile marker genes in the aorta including the genes encoding SM-α-actin (Acta2), calponin (Cnn1), SM-myosin heavy chain (Myh11) and β1-subunit of maxiK channel (Kcnmb1).
DTNA encodes α-dystrobrevin.
ACTA2 and MYH11 encode the smooth muscle cell specific α-actin and β-myosin heavy chain, respectively.
At the molecular level, cardiomyocyte hypertrophy is characterized by reinduction of the so-called fetal gene program, leading to upregulation of genes encoding atrial and brain natriuretic peptides, β-myosin heavy chain and skeletal α-actin [ 4].
In the vast majority of cases, these genes encode for sarcomeric contractile proteins such as troponin T (TNNT2), troponin I (TNNI3), and cardiac α-actin (ACTC) [ 7, 8].
The reporter plasmid encoding full-length luciferase under control of 424 basepairs upstream of the transcription start site of the chicken skeletal α-actin gene [ 59] was a gift from Dr. Frank W. Booth (University of Missouri, Columbia, USA).
