The 3′ Untranslated Region Protects the Heart from Angiotensin II-Induced Cardiac Dysfunction via AGGF1 Expression

Ding, Lexi; Lü, Shan; Zhou, Yu; Lyu, Dayin; Chen, Ouyang; Ma, Zhuo; Lu, Qiulun

doi:10.1016/j.ymthe.2020.02.002

Cited by 13 publications

(9 citation statements)

References 27 publications

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“…The mechanism underlying how Mcl1 3 -UTR regulates Mcl1 expression is due to microRNAs. We previously reported that the cluster microRNAs, including miR-93, miR-101, and miR-105, can recognize and bind with the 3 -UTR of Mcl1 and Aggf1 mRNAs (Ding et al, 2020). In vitro characterization corroborated Aggf1 as a Mcl1 ceRNA and showed that these genes share 3 -UTR binding sites for the same miRNAs, including miR-105, miR-101, and miR-93, which were upregulated in response to Ang II.…”

Section: Discussionmentioning

confidence: 86%

The Anti-apoptotic Role of 3′-Untranslational Region in Response to Angiotensin II via Mcl1 Expression

Lyu

Yan

Chen

et al. 2021

Front. Cell Dev. Biol.

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Myeloid cell leukemia 1 (Mcl1), an abundant protein in the myocardium, plays an essential role in fibrosis and anti-inflammation in cardiomyocytes to prevent heart failure. However, whether Mcl1 3′-untranslated regions (3′-UTR) has the cardio-protecting function remains unclear. Down-regulation of Mcl1 was observed in adult mice heart tissues after Angiotensin II (Ang II) treatment. Consistent with in vivo results, the reduction of Mcl1 expression was identified in Ang II-treated neonatal cardiomyocytes. Mechanistically, Mcl1 3′-UTR prevented Ang II-induced cardiac apoptosis via up-regulation of Mcl1 and an angiogenic factor with a G-patch domain and a forkhead-associated domain 1 (Aggf1), which plays cardiac-protective role. Our work broadens the scope of gene therapy targets and provides a new insight into gene therapy strategies involving mRNAs’ 3′-UTRs application.

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Section: Discussionmentioning

confidence: 86%

The Anti-apoptotic Role of 3′-Untranslational Region in Response to Angiotensin II via Mcl1 Expression

Lyu

Yan

Chen

et al. 2021

Front. Cell Dev. Biol.

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“…TUNEL staining was performed as previously report (18). The suitable density H9C2 cells were induced to CoCl 2 (100 uM, Sigma, 449776) under the condition of treatment with dioscin (5 mg/L) for 48 h, compared to control group.…”

Section: Tunel Stainingmentioning

confidence: 99%

Dioscin Alleviates Cardiac Dysfunction in Acute Myocardial Infarction via Rescuing Mitochondrial Malfunction

Shen

Lyu

Zhang

et al. 2022

Front. Cardiovasc. Med.

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Myocardial infarction is one of the most severe heart diseases, leading to sudden death. Currently, angiography and stenting are widely performed in clinics, yet more effective treatment is still needed. Herein, we presented that dioscin, a natural product, showed protective effect on infarcted hearts via mitochondrial maintenance. Upon dioscin treatment, cardiac dysfunction was alleviated, and remodeling is prevented. Mechanistically, disocin maintains mitochondria function through the maintenance of Kreb's cycle, and suppresion of ROS accumulation. In this way, by targeting mitochondrial dysfunction, dioscin is a potential drug for infarcted hearts.

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“…We Oxidative Medicine and Cellular Longevity 3.6. miR-133a Blunted PVF Proliferation and Activation. miRNAs control structural changes in the extracellular matrix of the myocardium [17,36]. miR-133a is decreased in pathological left ventricular hypertrophy [23], and miR-133a limits the production of CTGF and COL1A1 by directly targeting their 3′-UTR regions [20,23,37].…”

Section: Ivabradine Inhibited Cardiac Fibroblast Activation Andmentioning

confidence: 99%

“…Emerging evidence demonstrates that microRNAs (miR-NAs) play an important role in transcription and translation modification in myocardial hypertrophy and fibrosis-related gene expression [16,17]. miR-133a is highly expressed in the myocardium and regulates cardiac hypertrophy and myocardial fibrosis [18][19][20][21][22].…”

Section: Introductionmentioning

confidence: 99%

Ivabradine Ameliorates Cardiac Function in Heart Failure with Preserved and Reduced Ejection Fraction via Upregulation of miR‐133a

Shao

Zhang

Gong

et al. 2021

Oxidative Medicine and Cellular Longevity

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Heart failure (HF) is a clinical syndrome caused by impairment of ventricular filling, ejection of blood, or both and is categorized as HF with reduced ejection fraction (HFrEF) or HF with preserved ejection fraction (HFpEF) based on left ventricular function. Cardiac fibrosis contributes to left ventricular dysfunction and leads to the development of HF. Ivabradine, an If current selective specific inhibitor, has been shown to improve the prognosis of patients with HF. However, the effects of ivabradine on cardiac function and fibrosis in HFpEF and HFrEF and the underlying mechanism remain unclear. In the present study, we utilized mouse models to mimic HFpEF and HFrEF and evaluated the therapeutic effects of ivabradine. By treating mice with different doses (10 mg/kg/d and 20 mg/kg/d) of ivabradine for 4 or 8 weeks, we found that a high dose of ivabradine improved cardiac diastolic function in HFpEF mice and ameliorated cardiac diastolic and systolic function and ventricular tachycardia incidence in HFrEF mice. Moreover, ivabradine significantly reduced the activation of cardiac fibroblasts and myocardial fibrosis in mice. Mechanistically, microRNA-133a, which was upregulated by ivabradine, targeted connective tissue growth factor and collagen 1 in cardiac fibroblasts and might contribute to the protective role of ivabradine. Together, our work utilized mouse models to study HFpEF and HFrEF, demonstrated the protective role of ivabradine in HFpEF and HFrEF, and elucidated the potential underlying mechanism, which provides an effective strategy for related diseases.

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The 3′ Untranslated Region Protects the Heart from Angiotensin II-Induced Cardiac Dysfunction via AGGF1 Expression

Cited by 13 publications

References 27 publications

The Anti-apoptotic Role of 3′-Untranslational Region in Response to Angiotensin II via Mcl1 Expression

The Anti-apoptotic Role of 3′-Untranslational Region in Response to Angiotensin II via Mcl1 Expression

Dioscin Alleviates Cardiac Dysfunction in Acute Myocardial Infarction via Rescuing Mitochondrial Malfunction

Ivabradine Ameliorates Cardiac Function in Heart Failure with Preserved and Reduced Ejection Fraction via Upregulation of miR‐133a

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