Disease relevance of Bmyo

• Expression of sarcoplasmic/endoplasmic reticulum Ca2+-ATPase (SERCA)-2a and alpha-myosin heavy chain were reduced in hypothyroidism, whereas phospholamban and beta-myosin heavy chain were increased [1].
• The cardiac beta-myosin heavy chain isogene is induced selectively in alpha 1-adrenergic receptor-stimulated hypertrophy of cultured rat heart myocytes [2].
• Northern blot analysis showed an increase in beta-myosin heavy chain expression in the hearts of the sedentary infarction group soon after infarction when compared to sham controls [3].
• BACKGROUND: Reexpression of the fetal beta-myosin heavy chain (beta-MHC) gene was reported to be a marker for phenotypic reprogramming and cardiac hypertrophy in rats [4].
• cis-Acting sequences that mediate induction of beta-myosin heavy chain gene expression during left ventricular hypertrophy due to aortic constriction [5].

Psychiatry related information on Bmyo

• In contrast, there was no relationship between either beta-myosin heavy chain or cytochrome C oxidase expression and locomotor activity [6].

High impact information on Bmyo

• Sarcoplasmic reticulum Ca2+-ATPase (SERCA), phospholamban, and alpha- and beta-myosin heavy chain (MHC) proteins were assayed in homogenates of myocytes isolated from the same hearts [7].
• However, with exercise training, there was a significant attenuation of the beta-myosin heavy chain expression in the myocardium [3].
• The "fetal" beta-myosin heavy chain (MHC) was up-regulated about four-fold, whereas the "adult" alpha MHC was inhibited greater than 50-60%; expression of alpha-skeletal actin increased approximately two-fold, with little or no change in alpha-cardiac actin [8].
• Dissociation of left ventricular hypertrophy, beta-myosin heavy chain gene expression, and myosin isoform switch in rats after ascending aortic stenosis [4].
• METHODS AND RESULTS: The left ventricular expression of a directly injected reporter gene driven by 3542 bp of rat beta-myosin heavy chain (beta-MHC) promoter was increased 3.0-fold by aortic constriction (P<.005), an increment similar to the 3.2-fold increase in the level of the endogenous beta-MHC mRNA in the same left ventricles [5].

Chemical compound and disease context of Bmyo

• RNA analyses indicate that ventricles of clenbuterol-treated rats express elevated levels of mRNA to atrial natriuretic factor without a concomitant increase in skeletal alpha-actin and beta-myosin heavy chain, consistent with a "physiological" form of cardiac hypertrophy [9].
• Although both agents attenuated beta-myosin heavy chain expression, a marker of hypertrophy, losartan had a greater effect [10].
• In addition, the expression levels of skeletal alpha-actin, beta-myosin heavy chain, and ANP genes, markers of hypertrophy, were partially elevated by treatment with HS-142-1 (100 microg/mL) under nonstimulated or PE-stimulated conditions [11].
• Regulation of beta myosin heavy chain, c-myc and c-fos proto-oncogenes in thyroid hormone-induced hypertrophy of the rat myocardium [12].
• These data indicate that trilinolein inhibits angiotensin II-induced cardiomyocyte hypertrophy and beta-myosin heavy chain promoter activity via attenuation of reactive oxygen species generation [13].

Biological context of Bmyo

• Impact of beta-myosin heavy chain isoform expression on cross-bridge cycling kinetics [14].
• Alpha1-adrenergic receptor stimulation induces cardiac myocytes to hypertrophy and reactivates many fetal genes, including beta-myosin heavy chain (betaMyHC) and skeletal alpha-actin (SKA), by signaling through myocyte-specific CAT (M-CAT) cis elements, binding sites of the transcriptional enhancer factor-1 (TEF-1) family of transcription factors [15].
• Both compounds inhibited ET-1 and PE-induced protein synthesis and increased cell size, sarcomeric reorganization, and expression of beta-myosin heavy chain in myocytes with IC(50) values of 1-2 microm [16].
• This transactivation was dependent on sequence-specific binding of GATA-5 to the beta-myosin heavy chain GATA element [17].
• To understand the molecular basis for this functional difference, we determined the complete nucleotide sequence of full-length rat alpha and beta myosin heavy chain cDNAs [18].

Anatomical context of Bmyo

• Thus, the levels of expression of beta-myosin heavy chain and atrial natriuretic factor mRNA increased, of sarcoplasmic/endoplasmic reticulum ATPase (SERCA2) mRNA decreased, and of alpha-myosin heavy chain, phospholamban, and calsequestrin mRNA did not change [19].
• Although PO and VO caused comparable increases in LV weight and preproatrial natriuretic factor mRNA, PO but not VO increased mRNA levels for the fetal genes beta-myosin heavy chain and skeletal alpha-actin and reduced the mRNA level of sarcoplasmic reticulum Ca2+ATPase [20].
• In adult skeletal muscle, beta myosin heavy chain (betaMyHC) gene expression is primarily restricted to slow type I fibers; however, its expression is down-regulated in response to muscle inactivity [21].
• Myofibril regeneration, isoprotein transition of alpha- and beta-myosin heavy chain (MHC), and M-band localization of M-creatine kinase in the reconstituting heart cells were studied [22].
• An absent or negative inotropic response to isoproterenol is observed in SHR-F and SHR-NF papillary muscles and may result in part from age-related alterations in beta-adrenergic receptor dynamics and a shift from alpha- to beta-myosin heavy chain (MHC) protein [23].

Associations of Bmyo with chemical compounds

• Bosentan attenuated norepinephrine-induced increases in ventricular weight, ratio of RNA to protein, and expression of skeletal alpha-actin mRNA and beta-myosin heavy chain mRNA at 5 days, but it did not attenuate increased ventricular expression of atrial natriuretic factor mRNA [24].
• Moreover, rapamycin did not suppress Ang II-induced phenotypic changes at the protein level, such as increased atrial natriuretic factor secretion, expression of beta-myosin heavy chain, and organization of actin into sarcomeric units [25].
• The isoform ratio of beta-myosin heavy chain messenger ribonucleic acid quantitated by S1 nuclease mapping also was lower (p < 0.025) in rats receiving monocrotaline plus FR139317 than in those receiving monocrotaline alone [26].
• Candesartan and cilazapril significantly suppressed increased mRNA expression of beta-myosin heavy chain, alpha-skeletal actin, and atrial natriuretic peptide in noninfarcted ventricle at 1 and 4 weeks and expression of collagen I and III at 4 weeks to a similar extent [27].
• Amlodipine, but not nifedipine, prevented an increase in the relative amount of V3 myosin heavy chain isoform and suppressed an increase in mRNA levels of beta-myosin heavy chain, skeletal alpha-actin, and type 1 collagen [28].

Regulatory relationships of Bmyo

• In addition, NO also significantly inhibited ET-1-stimulated promoter activity of hypertrophic marker gene beta-myosin heavy chain and the enhanced protein synthesis [29].
• Pretreatment of myocytes with staurosporine also reduced the myotrophin-induced mRNA levels of c-fos and beta-myosin heavy chain [30].
• An exception is the skeletal muscle, where HSP 72 is constitutively expressed in muscles that express the beta myosin heavy chain (beta-MHC) protein [31].
• 3. After treatment with lipopolysaccharide, mRNA for beta-myosin heavy chain increased to 260% of control values at 24 h and reached a maximum of 310% at 48 h. alpha-Myosin heavy chain mRNA levels fell to 72% of control values at 24 h. mRNA levels for alpha-actin, cardiac troponin C and carbonic anhydrase III remained unchanged [32].

Other interactions of Bmyo

• Both beta-myosin heavy chain and skeletal alpha-actin expression were increased at all post-MI time points [33].
• Moreover, experiments performed with the specific JNK inhibitor SP-600125 abolished c-Jun phosphorylation and markedly attenuated its expression as well as the expression of the fetal gene beta-myosin heavy chain [34].
• Transfection of NRVMs with RhoA antisense oligonucleotide attenuated stretch-induced FAK and ERK1/2 phosphorylation and expression of beta-myosin heavy chain mRNA [35].
• The activation of the TGF-beta1-TAK1-p38 MAPK pathway paralleled the transcriptional upregulation of cardiac markers for ventricular hypertrophy, beta-myosin heavy chain and atrial natriuretic peptide [36].
• This response was associated with increased mRNA levels of atrial natriuretic factor, alpha- and beta-myosin heavy chain measured by RNase protection assay, and it was suppressed by the mineralocorticoid receptor blocker spironolactone [37].

Analytical, diagnostic and therapeutic context of Bmyo

• Consistent with a transcriptional mechanism, electrical stimulation increased c-fos, beta-myosin heavy chain, and Cyt c promoter activities [38].
• 35S-Labeled complementary RNA (cRNA) probes and in situ hybridization procedures were used for analysis of the regional distribution of newly formed transcripts from alpha-skeletal actin (alpha-sk-actin) and beta-myosin heavy chain (beta-MHC) genes during the early stages of pressure overload [39].
• SDS-PAGE and Western blot analysis showed that whereas myosin heavy chain expression underwent a transition to predominance of the early development isoform, beta-myosin heavy chain, there was no reexpression of the fetal isoforms of either troponin I or troponin T in the rat heart at 24 months of age [40].
• We developed an RT-PCR assay to study both the time course and the mechanism for the triiodothyronine (T(3))-induced transcription of the alpha- and beta-myosin heavy chain (MHC) genes in vivo on the basis of the quantity of specific heterogeneous nuclear RNA (hnRNA) [41].
• No differences existed in the profile of myosin protein isoforms or beta-myosin heavy chain mRNA in hearts between the flight and synchronous control groups [42].

References