Downregulation of miR-122 attenuates hypoxia/reoxygenation (H/R)-induced myocardial cell apoptosis by upregulating GATA-4

Liang, Wanqian; Guo, Jianxin; Li, Jianhua; Bai, Caiyan; Dong, Yuan

doi:10.1016/j.bbrc.2016.08.139

Cited by 37 publications

(24 citation statements)

References 25 publications

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“…For example, miR-7a-5p attenuates post-myocardial infarction remodeling and protects cardiac myocyte from hypoxia-induced apoptosis involving Sp1 and PARP-1 in mice [36-38] and miR-25 protects against hypoxia/reoxygenation-induced fibrosis and apoptosis in cardiomyocytes by targeting HMGB1 [39]. Also, miR-26 is induced in response to low oxygen and decreases proapoptotic signaling in a hypoxic environment [40], while miR-122-5p inhibition attenuates hypoxia/reoxygenation-induced myocardial cell apoptosis by targeting GATA4 [41]. There is also evidence showing that miR-145-5p is downregulated by ischaemia in acute myocardial infarction via targeting Dab2 [42] and miR-181a-5p is involved in hypoxia-induced chemoresistance in gastric cancer [43].…”

Section: Discussionmentioning

confidence: 99%

Characteristic MicroRNA Expression Induced by δ-Opioid Receptor Activation in the Rat Liver Under Prolonged Hypoxia

Zhi

Shao

Xue

et al. 2017

Cell Physiol Biochem

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Background/Aims: Hypoxic/ischemic injury to the liver is a frequently encountered clinical problem with limited therapeutic options. Since microRNAs (miRNAs) are involved in hypoxic/ ischemic events, and δ-opioid receptor (DOR) is protective against hypoxic/ischemic injury, we asked if pharmacological activation of DOR can alter hypoxic events by regulating miRNA expression in the liver. As the first step, the present work aimed at testing the effect of DOR activation on hepatic miRNA expression in hypoxia. Methods: Male Sprague Dawley rats were exposed to hypoxia (9.5-10% O₂) for 1, 5, or 10 days with or without DOR activation. The target miRNAs were selected according to TaqMan low-density array (TLDA) data and analyzed by quantitative real-time PCR. Results: We found that: 1) 1-day hypoxia caused the upregulation of 9 miRNAs (miR-7a-5p, miR-10a-5p, miR-25-3p, miR-26b-5p, miR-122-5p, miR-128a-3p, miR-135b-5p, miR-145-5p, and miR-181a-5p) and the downregulation of 2 miRNAs (miR-34a-5p and miR-182); 2) 5 and 10-days hypoxia altered the expression of 4 miRNAs (miR-34c-5p, miR-184, miR-107-3p and miR192-5p); 3) DOR activation shifted the expression of 8 miRNAs (miR-122-5p, miR-146a-5p, miR-30e-5p, miR-128a-3p, miR-182, miR-192-5p miR-107-3p and miR-184) in normoxic condition; and 4) DOR activation modified hypoxia-induced changes in 6 miRNAs (miR-142-5p, miR-145-5p, miR-146a-5p, miR-204-5p, miR-34a-5p and miR-192-5p). Conclusion: Hypoxia significantly modifies the miRNA profile in the liver, while DOR activation can modify the hypoxic modification. Therefore, it is potentially possible to alter hypoxic/ischemic pathophysiology in the liver through DOR pharmacotherapy.

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Section: Discussionmentioning

confidence: 99%

Characteristic MicroRNA Expression Induced by δ-Opioid Receptor Activation in the Rat Liver Under Prolonged Hypoxia

Zhi

Shao

Xue

et al. 2017

Cell Physiol Biochem

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“…Surprisingly, the levels of circulating exosomal miR-122 were positively associated with cardiac dysfunction in patients with HF with a reduced left ventricle (LV) ejection fraction (EF) and elevated levels of NT-proBNP [36]. A recent study demonstrated that miR-122 was highly expressed in cultured H9C2 cells under hypoxia/reoxygenation, and overexpression of miR-122 by recombinant adeno-associated infection significantly augmented the apoptosis of H9C2 cells [37]. In contrast, inhibition of miR-122 attenuated pathological cardiac remodeling and decreased cell apoptosis in myocardial ischemic injury [37].…”

Section: Mir-122 and Cardiovascular Fibrosis And Remodelingmentioning

confidence: 99%

“…A recent study demonstrated that miR-122 was highly expressed in cultured H9C2 cells under hypoxia/reoxygenation, and overexpression of miR-122 by recombinant adeno-associated infection significantly augmented the apoptosis of H9C2 cells [37]. In contrast, inhibition of miR-122 attenuated pathological cardiac remodeling and decreased cell apoptosis in myocardial ischemic injury [37]. In cultured neonatal rat ventricular myocytes (NRVMs), overexpression of miR-122 by miR-122 mimics increased the size of CMs and hypertrophic gene expression, but downregulated the expression of anti-hypertrophic genes upon Ang II stimulation (Table 1) [18].…”

Section: Mir-122 and Cardiovascular Fibrosis And Remodelingmentioning

confidence: 99%

Roles of MicroRNA-122 in Cardiovascular Fibrosis and Related Diseases

et al. 2020

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Fibrotic diseases cause annually more than 800,000 deaths worldwide, where of the majority accounts for cardiovascular fibrosis, which is characterized by endothelial dysfunction, myocardial stiffening and reduced dispensability. MicroRNAs (miRs), small noncoding RNAs, play critical roles in cardiovascular dysfunction and related disorders. Intriguingly, there is a critical link among miR-122, cardiovascular fibrosis, sirtuin 6 (SIRT6) and angiotensin-converting enzyme 2 (ACE2), which was recently identified as a coreceptor for SARS-CoV2 and a negative regulator of the rennin-angiotensin system. MiR-122 overexpression appears to exacerbate the angiotensin II-mediated loss of autophagy and increased inflammation, apoptosis, extracellular matrix deposition, cardiovascular fibrosis and dysfunction by modulating the SIRT6-Elabela-ACE2, LGR4-β-catenin, TGFβ-CTGF and PTEN-PI3K-Akt signaling pathways. More importantly, the inhibition of miR-122 has proautophagic, antioxidant, anti-inflammatory, anti-apoptotic and antifibrotic effects. Clinical and experimental studies clearly demonstrate that miR-122 functions as a crucial hallmark of fibrogenesis, cardiovascular injury and dysfunction. Additionally, the miR-122 level is related to the severity of hypertension, atherosclerosis, atrial fibrillation, acute myocardial infarction and heart failure, and miR-122 expression is a risk factor for these diseases. The miR-122 level has emerged as an early-warning biomarker cardiovascular fibrosis, and targeting miR-122 is a novel therapeutic approach against progression of cardiovascular dysfunction. Therefore, an increased understanding of the cardiovascular roles of miR-122 will help the development of effective interventions. This review summarizes the biogenesis of miR-122; regulatory effects and underlying mechanisms of miR-122 on cardiovascular fibrosis and related diseases; and its function as a potential specific biomarker for cardiovascular dysfunction.

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“…Inhibition of miR-320 up-regulates the level of IGF1 mRNA [47]. Likewise, the knockdown of miR-122, an apoptosis-related microRNA, attenuates hypoxia/reoxygenation-induced myocardial cell apoptosis by upregulating GATA-4 [48]. In oxidative stress condition, the expression of miR‑153 is significantly increased, and inhibition of endogenous miR‑153 can block cardiomyocyte apoptosis [49].…”

Section: Specific Function Of Micrornas In Cardiac Cell Deathmentioning

confidence: 99%

The Role of MicroRNAs in Myocardial Infarction: From Molecular Mechanism to Clinical Application

Sun

Dong

et al. 2017

IJMS

143

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MicroRNAs (miRNAs) are a class of small single-stranded and highly conserved non-coding RNAs, which are closely linked to cardiac disorders such as myocardial infarction (MI), cardiomyocyte hypertrophy, and heart failure. A growing number of studies have demonstrated that miRNAs determine the fate of the heart by regulating cardiac cell death and regeneration after MI. A deep understanding of the pathophysiology of miRNA dependent regulatory pathways in these processes is required. The role of miRNAs as diagnostic, prognostic, and therapeutic targets also needs to be explored in order to utilize them in clinical settings. This review summarizes the role of miRNAs in myocardial infarction and focuses mainly on their influence on cardiomyocyte regeneration and cell death including apoptosis, necrosis, and autophagy. In addition, the targets of pro- and anti-MI miRNAs are comparatively described. In particular, the possibilities of miRNA-based diagnostic and therapeutic strategies for myocardial infarction are discussed in this review.

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Downregulation of miR-122 attenuates hypoxia/reoxygenation (H/R)-induced myocardial cell apoptosis by upregulating GATA-4

Cited by 37 publications

References 25 publications

Characteristic MicroRNA Expression Induced by δ-Opioid Receptor Activation in the Rat Liver Under Prolonged Hypoxia

Characteristic MicroRNA Expression Induced by δ-Opioid Receptor Activation in the Rat Liver Under Prolonged Hypoxia

Roles of MicroRNA-122 in Cardiovascular Fibrosis and Related Diseases

The Role of MicroRNAs in Myocardial Infarction: From Molecular Mechanism to Clinical Application

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