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- W2022863690 abstract "Previously we have reported that hydrogen sulfide (H 2 S) protects against chronic heart failure, and elevated level of homocysteine (Hcy) called hyperhomocysteinemia (HHcy, a co-morbid condition) exacerbates diabetic cardiomyopathy. The generation of H 2 S from Hcy requires cystathionine γ -lyase (CBS) enzyme and mutation of CBS (CBS+/−) causes pathological cardiac remodeling. Since miR-133a (cardiac fibrosis) and β 2-adrenergic receptors ( β 2-AR: contractile dysfunction) are attenuated in diabetic hearts and contribute to cardiac remodeling, we hypothesize that inhibition of CBS induces HHcy and attenuates miR-133a and β 2-AR due to decreased production of H 2 S. To prove the hypothesis, we used C57BL/6 J (WT), CBS+/− with and without NaHS (a H 2 S donor, 30 μM/L in drinking water for 4 weeks) and measured the levels of miR-133a and β 2-AR by individual miR-133a assay, multiplex RT-PCR and Western blotting. Additionally, to assess the role of H 2 S in mitigation of glucose mediated inhibition of β 2-AR, we determined the levels of stimulatory G -protein coupled receptor (Gs: inducer of β 2-AR) and β 2-AR in HL1 cardiomyocytes treated with high glucose (25 mM D-glucose) and high glucose + H 2 S (30 μM) by RT-PCR flow cytometry and RT-PCR. The results revealed that both miR-133a and β 2-AR are down regulated in CBS+/− hearts. However, treatment with H 2 S improves the levels of miR-133a and β 2-AR. Similarly, Gs and β 2-AR are down regulated in high glucose treated cardiomyocytes and H 2 S ameliorates both Gs and β 2-AR. These findings elicit that H 2 S induces miR-133a and β 2-AR in HHcy hearts and ameliorates diabetic cardiomyopathy." @default.
- W2022863690 created "2016-06-24" @default.
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- W2022863690 date "2012-09-01" @default.
- W2022863690 modified "2023-09-26" @default.
- W2022863690 title "P59 H2S ameliorates homocysteine mediated attenuation of miR-133a and β2-AR in diabetic hearts" @default.
- W2022863690 doi "https://doi.org/10.1016/j.niox.2012.08.060" @default.
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