Hydrogen sulphide inhibits cardiomyocyte hypertrophy by up-regulating miR-133a

Li, Jun; Hao, Dandan; Zhang, Jinsheng; Zhu, Yi‐Chun

doi:10.1016/j.bbrc.2011.08.101

Cited by 52 publications

(34 citation statements)

References 26 publications

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“…Since miR-133a is recognized as an anti-hypertrophy miRNA [24], and H 2 S is reported to induce miR-133a [30], we were interested to evaluate the effect of HHcy on miR-133a in cardiomyocytes. For that, we measured the levels of miR-133a in the above-mentioned four groups using individual miR-133a assay as described elsewhere [31].…”

Section: Resultsmentioning

confidence: 99%

Hydrogen sulfide mitigates homocysteine-mediated pathological remodeling by inducing miR-133a in cardiomyocytes

et al. 2015

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An elevated level of homocysteine called hyperhomocysteinemia (HHcy) is associated with pathological cardiac remodeling. Hydrogen sulfide (H2S) acts as a cardioprotective gas, however the mechanism by which H2S mitigates homocysteine mediated pathological remodeling in cardiomyocytes is unclear. We hypothesized that H2S ameliorates HHcy mediated hypertrophy by inducing cardioprotective miR-133a in cardiomyocytes. To test the hypothesis, HL1 cardiomyocytes were treated with: 1) plain medium (control, CT), 2) 100μM of homocysteine (Hcy), 3) Hcy with 30μM of H2S (Hcy+H2S), and 4) H2S for 24 hour. The levels of hypertrophy markers: c-fos, atrial natriuretic peptide (ANP), and beta-myosin heavy chain (β-MHC), miR-133a and its transcriptional inducer myosin enhancer factor- 2c (MEF2C) were determined by Western blotting, RT-qPCR, and immunofluorescence. The activity of MEF2C was assessed by co-immunoprecipitation of MEF2C with histone deacetylase -1(HDAC1). Our results show that H2S ameliorates homocysteine mediated up regulation of c-fos, ANP and β-MHC, and down regulation of MEF2C and miR-133a. HHcy induces the binding of MEF2C with HDAC1, whereas H2S releases MEF2C from MEF2C-HDAC1 complex causing activation of MEF2C. These findings elicit that HHcy induces cardiac hypertrophy by promoting MEF2C-HDAC1 complex formation that inactivates MEF2C causing suppression of anti-hypertrophy miR-133a in cardiomyocytes. H2S mitigates hypertrophy by inducing miR-133a through activation of MEF2C in HHcy cardiomyocytes. To our knowledge this is a novel mechanism of H2S mediated activation of MEF2C and induction of miR-133a and inhibition of hypertrophy in HHcy cardiomyocytes.

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Section: Resultsmentioning

confidence: 99%

Hydrogen sulfide mitigates homocysteine-mediated pathological remodeling by inducing miR-133a in cardiomyocytes

et al. 2015

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“…MiRNAs are rapidly emerging as therapeutic targets for CVD (22,103,108,122,126). H 2 S regulates miRNA expression (70,73,93); however, the interaction between H 2 S and miRNAs in CVD is poorly understood. Only a few publications document that miRNAs may regulate enzymes that control H 2 S biosynthesis and that H 2 S regulates miRNAs.…”

Section: H 2 S Mitigates Pathological Cardiac Remodeling By Inhibitinmentioning

confidence: 99%

“…Not only do miRNAs regulate the biosynthesis of H 2 S, but H 2 S has also been demonstrated to regulate miRNAs. NaHS (100 M) treatment upregulates cardioprotective miR-133a in primary cultures of neonatal rat cardiomyocytes to inhibit phenylepinephrine-induced cardiomyocyte hypertrophy (93). Furthermore, Na 2 S (30 M) treatment increased miR-133a level to suppress hyperhomocysteinemia-induced cardiomyocyte hypertrophy in HL1 cardiomyocytes (73).…”

Section: H 2 S Mitigates Pathological Cardiac Remodeling By Inhibitinmentioning

confidence: 99%

“…The interaction of H 2 S with miRNA is recently uncovered and is an emerging area of investigation. An example of H 2 S-miRNA crosstalk is that H 2 S downregulates miR-21 to mitigate phenylephrine-induced cardiomyocyte hypertrophy (93), and miR-21 targets SP1 to decrease CSE transcription and H 2 S production (157). Furthermore, increased miR-21 levels and decreased CSE levels are found in placental tissue from high risk pregnancy as compared with normal pregnancy, suggesting that low H 2 S level may induce miR-21 and contribute to increased pregnancy complications (32).…”

Section: H 2 S Mitigates Pathological Cardiac Remodeling By Inhibitinmentioning

confidence: 99%

“…Evidence is mounting that H 2 S is important in reducing the symptoms associated with CVD. H 2 S reduces hypertension (2, 3), improves glucose uptake and metabolism (9, 89), protects against ischemia-reperfusion (I/R) injury (70,81,141,161), and decreases cardiac hypertrophy (9,73,93,97). Further evidence shows that free H 2 S levels are reduced in patients with CVD (64,79,118), suggesting H 2 S supplementation may be a potential therapy for mitigating CVD.…”

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confidence: 99%

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Emerging role of hydrogen sulfide-microRNA crosstalk in cardiovascular diseases

Hackfort

Mishra

2016

American Journal of Physiology-Heart and Circulatory Physiology

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Protective Actions of H₂S in Acute Myocardial Infarction and Heart Failure

Donnarumma

Trivedi

Lefer

2017

Comprehensive Physiology

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Hydrogen sulfide (H2S) was identified as the third gasotransmitter in 1996 following the discoveries of the biological importance of nitric oxide and carbon monoxide. Although H2S has long been considered a highly toxic gas, the discovery of its presence and enzymatic production in mammalian tissues supports a critical role for this physiological signaling molecule. H2S is synthesized endogenously by three enzymes: cystathionine β-synthase, cystathionine-γ-lyase, and 3-mercaptopyruvate sulfurtransferase. H2S plays a pivotal role in the regulation of cardiovascular function as H2S has been shown to modulate: vasodilation, angiogenesis, inflammation, oxidative stress, and apoptosis. Perturbation of endogenous production of H2S has been associated with many pathological conditions of the cardiovascular system such as diabetes, heart failure, and hypertension. As such, modulation of the endogenous H2S signaling pathway or administration of exogenous H2S has been shown to be cytoprotective. This review article will provide a summary of the current body of evidence on the role of H2S signaling in the setting of myocardial ischemia and heart failure. © 2017 American Physiological Society. Compr Physiol 7:583-602, 2017.

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Hydrogen sulphide inhibits cardiomyocyte hypertrophy by up-regulating miR-133a

Cited by 52 publications

References 26 publications

Hydrogen sulfide mitigates homocysteine-mediated pathological remodeling by inducing miR-133a in cardiomyocytes

Hydrogen sulfide mitigates homocysteine-mediated pathological remodeling by inducing miR-133a in cardiomyocytes

Emerging role of hydrogen sulfide-microRNA crosstalk in cardiovascular diseases

Protective Actions of H₂S in Acute Myocardial Infarction and Heart Failure

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Hydrogen sulphide inhibits cardiomyocyte hypertrophy by up-regulating miR-133a

Cited by 52 publications

References 26 publications

Hydrogen sulfide mitigates homocysteine-mediated pathological remodeling by inducing miR-133a in cardiomyocytes

Hydrogen sulfide mitigates homocysteine-mediated pathological remodeling by inducing miR-133a in cardiomyocytes

Emerging role of hydrogen sulfide-microRNA crosstalk in cardiovascular diseases

Protective Actions of H2S in Acute Myocardial Infarction and Heart Failure

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Product

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Protective Actions of H₂S in Acute Myocardial Infarction and Heart Failure