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The myostatin gene inhibits skeletal muscle growth in advanced animals, and a mutation in the gene coding region increases muscle formation. Hence, it is accepted to be a candidate gene for the selection of some production traits. The objective of the current research was to examine the genotypes of the myostatin gene and reveal the associations between the genotypes and a number of traits, including birth weight, weaning weight, weaning age, average daily weight gain, and productivity, in 110 Morkaraman sheep. Genotypes were determined by the PCR-RFLP method using the HaeIII restriction enzyme, and the genotype frequencies were found to be 9%, 69%, and 22% for MM, Mm, and mm in the myostatin locus, respectively. The M allele frequency was 44%, whereas the m allele frequency was 56%. In the studied population, the myostatin locus was not in Hardy-Weinberg equilibrium. The association analysis revealed no statistically significant impact of the MSTN gene polymorphism in exon 3 on birth weight, weaning weight, and productivity (P>0.05) but found a significant effect on weaning age and average daily weight gain (P<0.05). As a result, the MSTN gene showed polymorphisms in Morkaraman sheep and can be regarded as a genetic marker for sheep selection according to the association analysis results. [ABSTRACT FROM AUTHOR]

The biomechanical environment to which cells are exposed is important to their normal growth, development, interaction, and function. Accordingly, there has been much interest in studying the role of biomechanical forces in cell biology and pathophysiology. This has led to the introduction and even commercialization of many experimental devices. Many of the early devices were limited by the heterogeneity of deformation of cells cultivated in different locations of the culture plate membranes and were also attached with complicated technical/electronic efforts resulting in a restriction of the reproducibility of these devices. The objective of this study was to design and build a simple device to allow the application of dose-dependent homogeneous equibiaxial static stretch to cells cultured on flexible silicone membranes to investigate biological and biomedical questions. In addition, cultured neonatal rat atrial cardiomyocytes were stretched with the proposed device with different strain gradients. For the first time with this study we could demonstrate that stretch up to 21% caused dose-dependent changes in biological markers such as the calcineurin activity, modulatory calcineurin-interacting protein-l, voltage-gated potassium channel isoform 4.2, and voltage-gated [K.sup.+] channel-interacting proteins-2 gene expression and transient outward potassium current densities but not the protein-to-DNA ratio and atrial natriuretic peptide mRNA. With both markers mentioned last, dose-dependent stretch alterations could only be achieved with stretch up to 13%. The simple and low-cost device presented here might be applied to a wide range of experimental settings in different fields of research. equibiaxial stretch; hypertrophy; calcineurin

Atrial fibrillation (AF) is the most frequent arrhythmia found in clinical practice. In recent studies, a decrease in the development or recurrence of AF was found in hypertensive patients treated with angiotensin-converting enzyme inhibitors or angiotensin receptor-blocking agents. Hypertension is related to an increased wall tension in the atria, resulting in increased stretch of the individual myocyte, which is one of the major stimuli for the remodeling process. In the present study, we used a model of cultured atrial neonatal rat cardiomyocytes under conditions of stretch to provide insight into the mechanisms of the preventive effect of the angiotensin receptor-blocking agent losartan against AF on a molecular level. Stretch significantly increased protein-to-DNA ratio and atrial natriuretic factor mRNA expression, indicating hypertrophy. Expression of genes encoding for the inward rectifier K+ current (IKI), Kir2.1, and Kir2.3, as well as the gene encoding for the ultrarapid delayed rectifier [K.sup.+] current ([I.sub.Kur]), Kv1.5, was significantly increased. In contrast, mRNA expression of Kv4.2 was significantly reduced in stretched myocytes. Alterations of gene expression correlated with the corresponding current densities: [I.sub.K1] and [I.sub.Kur] densities were significantly increased in stretched myocytes, whereas transient outward [K.sup.+] current ([I.sub.to]) density was reduced. These alterations resulted in a significant abbreviation of the action potential duration. Losartan (1 [micro]M) prevented stretch-induced increases in the protein-to-DNA ratio and atrial natriuretic peptide mRNA expression in stretched myocytes. Concomitantly, losartan attenuated stretch-induced alterations in [I.sub.K1], [I.sub.Kur], and [I.sub.to] density and gene expression. This prevented the stretch-induced abbreviation of action potential duration. Prevention of stretch-induced electrical remodeling might contribute to the clinical effects of losartan against AF. atrial fibrillation; mechanical stretch; hypertrophy; ion channels doi:10.1152/ajpheart.00546.2006

Atrial fibrillation (AF) is the most frequent arrhythmia found in clinical practice. In recent studies, a decrease in the development or recurrence of AF was found in hypertensive patients treated with angiotensin-converting enzyme inhibitors or angiotensin receptor-blocking agents. Hypertension is related to an increased wall tension in the atria, resulting in increased stretch of the individual myocyte, which is one of the major stimuli for the remodeling process. In the present study, we used a model of cultured atrial neonatal rat cardiomyocytes under conditions of stretch to provide insight into the mechanisms of the preventive effect of the angiotensin receptor-blocking agent losartan against AF on a molecular level. Stretch significantly increased protein-to-DNA ratio and atrial natriuretic factor mRNA expression, indicating hyper- trophy. Expression of genes encoding for the inward rectifier K+ current (IK1), Kir2.1, and Kir2.3, as well as the gene encoding for the ultrarapid delayed rectifier K+ current (IKur), Kv1.5, was significantly increased. In contrast, mRNA expression of Kv4.2 was significantly reduced in stretched myocytes. Alterations of gene expression correlated with the corresponding current densities: IK1 and IKur densities were significantly increased in stretched myocytes, whereas transient outward K+ current (Ito) density was reduced. These alterations resulted in a significant abbreviation of the action potential duration. Losartan (1 µM) prevented stretch-induced increases in the protein-to-DNA ratio and atrial natriuretic peptide mRNA expression in stretched myocytes. Concomitantly, losartan attenuated stretch-induced alterations in IK1, IKur, and Ito, density and gene expression. This prevented the stretch-induced abbreviation of action potential duration. Prevention of stretch-induced electrical remodeling might contribute to the clinical effects of losartan against AF. [ABSTRACT FROM AUTHOR]

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