Regulation of α- and β-myosin heavy chain messenger RNAs in the rat myocardium by amiodarone and by thyroid status

1989 ◽  
Vol 76 (5) ◽  
pp. 463-467 ◽  
Author(s):  
J. A. Franklyn ◽  
N. K. Green ◽  
M. D. Gammage ◽  
J. A. O. Ahlquist ◽  
M. C. Sheppard
Keyword(s):  
Gene Expression ◽  
Myosin Heavy Chain ◽  
Heavy Chain ◽  
Cdna Probe ◽  
Messenger Rnas ◽  
Thyroid Status ◽  
Dot Hybridization ◽  
Spot 14 ◽  
Amiodarone Treatment ◽  
Regulated Gene Expression

1. A number of the cardiovascular effects of amiodarone resemble those of hypothyroidism, prompting examination of the relationship between the actions of the drug and thyroid hormones. Amiodarone treatment of the rat was used as a model to determine the influence of the drug on thyroid hormone-regulated gene expression in the myocardium and liver; interactions between amiodarone and thyroid status were examined in hypothyroid and tri-iodothyronine (T3)-treated animals. 2. Myocardial levels of α- and β-myosin heavy chain (MHC) messenger RNAs (mRNAs) were measured by dot hybridization to specific oligonucleotide probes; myocardial actin mRNA was measured in parallel by hybridization to a complementary DNA (cDNA) probe. Hepatic levels of Spot 14 and thyroxine-binding prealbumin mRNA were similarly determined by dot hybridization to radiolabelled cDNAs. 3. Amiodarone treatment of the rat resulted in specific increases in both α- and β-MHC mRNAs in the myocardium, as well as hepatic Spot 14 mRNA, changes reversed by T3 administration. 4. Hypothyroidism resulted in a reduction in myocardial α-MHC and hepatic Spot 14 mRNAs, in contrast to amiodarone, whilst hypothyroidism and amiodarone both exerted stimulatory influences on β-MHC mRNA. Treatment of hypothyroid rats with amiodarone had no significant effect on β-MHC or Spot 14 mRNAs, but a further reduction in α-MHC mRNA, compared with the untreated hypothyroid state, was evident. 5. The demonstrated influence of amiodarone on both α- and β-MHC mRNAs and interactions between amiodarone and thyroid status in regulating MHC gene expression may be relevant to its therapeutic effect in man.

Expression of the atrial-specific myosin heavy chain AMHC1 and the establishment of anteroposterior polarity in the developing chicken heart

Development ◽  
1994 ◽  
Vol 120 (4) ◽  
pp. 871-883 ◽  
Author(s):  
K.E. Yutzey ◽  
J.T. Rhee ◽  
D. Bader
Keyword(s):  
Gene Expression ◽  
Retinoic Acid ◽  
Myosin Heavy Chain ◽  
Heavy Chain ◽  
Cardiac Myocyte ◽  
Anterior Segment ◽  
Heart Cells ◽  
Heart Tube ◽  
Expression Domain ◽  
Chicken Heart

A unique myosin heavy chain cDNA (AMHC1), which is expressed exclusively in the atria of the developing chicken heart, was isolated and used to study the generation of diversified cardiac myocyte cell lineages. The pattern of AMHC1 gene expression during heart formation was determined by whole-mount in situ hybridization. AMHC1 is first activated in the posterior segment of the heart when these myocytes initially differentiate (Hamburger and Hamilton stage 9+). The anterior segment of the heart at this stage does not express AMHC1 although the ventricular myosin heavy chain isoform is strongly expressed beginning at stage 8+. Throughout chicken development, AMHC1 continues to be expressed in the posterior heart tube as it develops into the diversified atria. The early activation of AMHC1 expression in the posterior cardiac myocytes suggests that the heart cells are diversified when they differentiate initially and that the anterior heart progenitors differ from the posterior heart progenitors in their myosin isoform gene expression. The expression domain of AMHC1 can be expanded anteriorly within the heart tube by treating embryos with retinoic acid as the heart primordia fuse. Embryos treated with retinoic acid prior to the initiation of fusion of the heart primordia express AMHC1 throughout the entire heart-forming region and fusion of the heart primordia is inhibited. These data indicate that retinoic acid treatment produces an expansion of the posterior (atrial) domain of the heart and suggests that diversified fates of cardiomyogenic progenitors can be altered.

Regulation of β myosin heavy chain, c-myc and c-fos proto-oncogenes in thyroid hormone-induced hypertrophy of the rat myocardium

1993 ◽  
Vol 84 (1) ◽  
pp. 61-67 ◽  
Author(s):  
N. K. Green ◽  
M. D. Gammage ◽  
J. A. Franklyn ◽  
A. M. Heagerty ◽  
M. C. Sheppard
Keyword(s):  
Thyroid Hormone ◽  
Right Ventricular ◽  
Myosin Heavy Chain ◽  
Heavy Chain ◽  
Molecular Mechanisms ◽  
Left Ventricular ◽  
Transcriptional Level ◽  
Messenger Rnas ◽  
Hypertrophic Response ◽  
Left And Right

1. In order to investigate the molecular mechanisms determining the hypertrophic response of the ventricular myocardium to thyroid hormone administration, changes in left and right ventricular expression of the c-myc, c-fos and H-ras proto-oncogenes in response to treatment with 3,3′,5-tri-iodothyronine were defined. 2. Adult female Wistar rats were treated with daily subcutaneous injections of 3,3′,5-tri-iodothyronine (50 μg) for 1, 3, 7 or 14 days (n = 6 in each treatment group) and the results from 3,3′,5-tri-iodothyronine-treated animals were compared with those obtained from untreated controls (n = 6). Changes in the weight of the left and right ventricles in response to 3,3′,5-tri-iodothyronine treatment were measured; changes in expression of the c-myc, c-fos and H-ras proto-oncogenes were determined in parallel by measurement of specific messenger RNAs by Northern and dot hybridization, as well as changes in expression of β myosin heavy chain messenger RNA. 3. Treatment with 3,3′,5-tri-iodothyronine resulted in increases in both left and right ventricular weights after 3 days, an effect maintained up to 14 days. Despite an increase in left ventricular weight, levels of β myosin heavy chain, c-myc, c-fos and H-ras mRNAs in the left ventricle were unchanged; in contrast, an increase in right ventricular weight was associated with increased expression of β myosin heavy chain, c-myc and c-fos messenger RNAs. 4. These specific ventricular changes in gene expression, in the face of a hypertrophic response of both ventricles to 3,3′,5-tri-iodothyronine, suggest that the cardiac growth response to thyroid hormones reflects the well-documented secondary haemodynamic influences rather than direct gene regulatory actions of 3,3′,5-tri-iodothyronine at the transcriptional level on the genes studied. Changes in right ventricular proto-oncogene and β myosin heavy chain expression may in turn reflect an increase in right ventricular pressure load.

bHLH transcription factor MyoD affects myosin heavy chain expression pattern in a muscle-specific fashion

2001 ◽  
Vol 280 (2) ◽  
pp. C408-C413 ◽  
Author(s):  
David J. Seward ◽  
John C. Haney ◽  
Michael A. Rudnicki ◽  
Steven J. Swoap
Keyword(s):  
Gene Expression ◽  
Myosin Heavy Chain ◽  
Heavy Chain ◽  
Biceps Brachii ◽  
Bhlh Transcription Factor ◽  
Hindlimb Unweighting ◽  
Protein Pool ◽  
In The Wild ◽  
Myod Gene ◽  
Mhc Iib

A strong correlative pattern between MyoD gene expression and myosin heavy chain IIB (MHC IIB) gene expression exists. To test whether this correlative relationship is causative, MHC gene expression in muscles from MyoD(−/−) mice was analyzed. The MHC IIB gene was not detectable in the MyoD(−/−) diaphragm, whereas the MHC IIB protein made up 10.0 ± 1.7% of the MHC protein pool in the wild-type (WT) mouse diaphragm. Furthermore, the MHC IIA protein was not detectable in the MyoD(−/−) biceps brachii, and the MHC IIB protein was overexpressed in the masseter. To examine whether MyoD is required for the upregulation of the MHC IIB gene within slow muscle after disuse, MyoD(−/−) and WT hindlimb musculature was unweighted. MyoD(−/−) exhibited a diminished response in the upregulation of the MHC IIB mRNA within the soleus muscle as a result of the hindlimb unweighting. Collectively, these data suggest that MyoD plays a role in the MHC profile in a muscle-specific fashion.

Effects of triiodo-thyronine on angiotensin-induced cardiomyocyte hypertrophy: reversal of increased β-myosin heavy chain gene expression

2006 ◽  
Vol 84 (8-9) ◽  
pp. 935-941 ◽  
Author(s):  
Baohua Wang ◽  
Jingping Ouyang ◽  
Zhengyuan Xia
Keyword(s):  
Gene Expression ◽  
Angiotensin Ii ◽  
Thyroid Hormone ◽  
Cardiac Hypertrophy ◽  
Atpase Activity ◽  
Mrna Expression ◽  
Myosin Heavy Chain ◽  
Heavy Chain ◽  
Ang Ii ◽  
Hypertrophic Growth

Thyroid hormone-induced cardiac hypertrophy is similar to that observed in physiological hypertrophy, which is associated with high cardiac contractility and increased α-myosin heavy chain (α-MHC, the high ATPase activity isoform) expression. In contrast, angiotensin II (Ang II) induces an increase in myocardial mass with a compromised contractility accompanied by a shift from α-MHC to the fetal isoform β-MHC (the low ATPase activity isoform), which is considered as a pathological hypertrophy and inevitably leads to the development of heart failure. The present study is designed to assess the effect of thyroid hormone on angiotensin II-induced hypertrophic growth of cardiomyocytes in vitro. Cardiomyocytes were prepared from hearts of neonatal Wistar rats. The effects of Ang II and 3,3′,5-triiodo-thyronine (T3) on incorporations of [3H]-thymine and [3H]-leucine, MHC isoform mRNA expression, PKC activity, and PKC isoform protein expression were studied. Ang II enhanced [3H]-leucine incorporation, β-MHC mRNA expression, PKC activity, and PKCε expression and inhibited α-MHC mRNA expression in cardiomyocytes. T3 treatment prevented Ang II-induced increases in PKC activity, PKCε, and β-MHC mRNA overexpression and favored α-MHC mRNA expression. Thyroid hormone appears to be able to reprogram gene expression in Ang II-induced cardiac hypertrophy, and a PKC signal pathway may be involved in such remodeling process.

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