Our study demonstrates that the expression of miR-30b-5p is down-regulated in cardiac hypertrophy, and restoration of its function inhibits the expression of CaMKIIδ, suggesting that miR-30b-5p may act as a hypertrophic suppressor.

OBJECTIVE: Expression of the Cacna1c(calcium channel, voltage-dependent, Ltype, a1C subunit) gene was studied to investigate the relationship between oxidative stress and L-type calcium channels in the myocardium of seleniumdeficient mice. METHODS: Selenium levels in liver and heart tissue samples from mice fed normal or selenium-deficient diets were evaluated by fluorometry. In the same mice, glutathione peroxidase (GPx) and Cacna1c gene expression were analysed, malondialdehyde (MDA) content and superoxide dismutase (SOD) activity were measured, oxidoreductase gene expression profiles were analysed (by DNA microarray), and myocardial structural changes were studied. RESULTS: In selenium-deficient versus control mice, Research has shown that deregulation of calcium through L-type calcium channels plays a crucial role in the pathogenesis of cell death, which results in calcium overload and eventually leads to cardiomyocyte injury. 5 Nevertheless, considerable uncertainty remains about whether L-type calcium channels are involved in cardiomyocyte damage induced by oxidative stress, and the degree to which the abundance and function of the L-type calcium channels are affected by oxidative stress. The present study assessed the relationship between oxidative stress and Ltype calcium channel levels in the myocardium, using a selenium-deficient mouse model. Materials and methods EXPERIMENTAL ANIMAL MODEL OF SELENIUM DEFICIENCYThe animal model of selenium deficiency was established according to the method of Vanderlelie et al. 6 , with slight modifications. The basal diet of the mice was low in selenium, containing 47% low-selenium yeast, 42% sucrose, 5% coconut oil, 5% premixed minerals and 1% premixed vitamins. Adult male and female C57BL/6 mice weighing 20 -25 g (10 weeks old) were housed in a pathogen-free environment at room temperature (22 -25°C) and maintained on the basal diet and tap water ad libitum before the selenium-deficient state was achieved. Animals were divided into six groups (n = 6 per group). Mice in seleniumdeficient groups were then fed a special mouse food that contained 4.5 µg/kg total selenium for 4, 12 or 24 weeks (groups SD-4w, SD-12w and SD-24w, respectively); control mice were fed standard mouse food containing 219 µg/kg total selenium for 4, 12 or 24 weeks (groups Ctr-4w, Ctr-12w and Ctr24w, respectively). At 4, 12 or 24 weeks, mice were sacrificed by severing the spinal cord. The heart, liver, brain and kidneys were perfused with ice-cold physiological saline (0.9% NaCl) until the blood was sufficiently removed; These organs were retained (and stored in ice-cold conditions) for use in the following experiments.Animal protocols were reviewed and approved by the Animal Care and Ethics

Cardiac hypertrophy is often associated with an increased sympathetic drive, and both in vitro and in vivo studies have demonstrated the development of cardiomyocyte hypertrophy in response to either α- or β- adrenergic stimulation. The present study was carried out to determine whether the reversible sodium channel blocker tetrodotoxin (TTX) exerts a direct anti-hypertrophic effect on isoproterenol (ISO)-induced cell hypertrophy and find the underlying mechanism that regulate [Na(+)]( i ). The experiments were performed on cultured H9c2 cells exposed to ISO (10 μM) alone or combined with TTX (1 μM) for 48 h. Our results showed that ISO significantly increased cell surface area by 30 % and atrial natriuretic peptide gene expression by nearly twofold (p < 0.05 for both). These effects were associated with a significant reduction in the gene expression of Na(+)/K(+)-ATPase isoforms α2 and α3, whereas the α1 isoform was unaffected. Conversely, ISO increased Na(+)-H(+) exchanger 1 (NHE-1) gene expression by approximately 40 % and significantly increased [Na(+)]( i ) level by 50 % (p < 0.05 for both). ISO was also found to significantly increase aquaporin 4 gene expression by nearly ninefold (p < 0.05). All these effects were prevented when identical experiments were carried out in the presence of TTX, but the expression of NHE-1. The expression of sodium channel protein type 5 subunit alpha was unaffected by either ISO or TTX. When taken together, these studies show that TTX attenuates the hypertrophic effect of ISO and suggest a possible approach to limiting ISO-induced hypertrophy in clinical treatment.