microRNA-200a-3p enhances mitochondrial elongation by targeting mitochondrial fission factor

Lee, Heejin; Tak, Hyosun; Park, Soo‐Young; Jo, Yoon Kyung; Cho, Dong Hyung; Lee, Eun Kyung

doi:10.5483/bmbrep.2017.50.4.006

Cited by 17 publications

(11 citation statements)

References 62 publications

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“…MiR-484 participates in mitochondrial network regulation by targeting Fis1, improving mitochondrial fission (Wang et al, 2012). In addition, miR-200a-3p and miR-761 can improve mitochondrial dysfunction by targeting the negative regulation of MFF, enhancing mitochondrial activity and ATP production (Long et al, 2013;Lee et al, 2017). MFN2mediated mitochondrial fusion is inhibited by miR-195, miR-20b, and miR-93 (Feng et al, 2019;Purohit et al, 2019;Qiu et al, 2020).…”

Section: Mitochondrial Dynamicsmentioning

confidence: 99%

MicroRNAs Regulating Mitochondrial Function in Cardiac Diseases

et al. 2021

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Mitochondria are the key organelles that supply cellular energy. As the most active organ in the body, the energy required to maintain the mechanical function of the heart requires a high quantity of high-quality mitochondria in cardiomyocytes. MicroRNAs (miRNAs) are single-stranded noncoding RNAs, approximately 22 nt in length, which play key roles in mediating post-transcriptional gene silencing. Numerous studies have confirmed that miRNAs can participate in the occurrence and development of cardiac diseases by regulating mitochondrial function-related genes and signaling pathways. Therefore, elucidating the crosstalk that occurs between miRNAs and mitochondria is important for the prevention and treatment of cardiac diseases. In this review, we discuss the biogenesis of miRNAs, the miRNA-mediated regulation of major genes involved in the maintenance of mitochondrial function, and the effects of miRNAs on mitochondrial function in cardiac diseases in order to provide a theoretical basis for the clinical prevention and treatment of cardiac disease and the development of new drugs.

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Section: Mitochondrial Dynamicsmentioning

confidence: 99%

MicroRNAs Regulating Mitochondrial Function in Cardiac Diseases

et al. 2021

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“…Thus, we detected several miRNAs under NA treatment. We checked the expressions of miR‐27, and miR‐200a‐3p, in response to NA treatment which target MFF to modulate mitochondrial network. The result showed there were no significantly alterations of miR‐27 or miR‐200a‐3p levels after NA treatment compared with control group (Supplement Figure A and B).…”

Section: Resultsmentioning

confidence: 99%

“…The equilibrium of dynamic is largely dependent on MFF balance, which is crucial for mitochondrial homeostasis and cell health. 15,18 Mitochondrial fission factor is known as a receptor to promote mitochondrial fission by recruitment Drp1 onto mitochondria membrane, 17,19 and alteration of expression of MFF is related with cardiovascular diseases. 10,[20][21][22] Mitochondrial fission factor is directly inhibited by miR-761 upon hydrogen peroxide treatment or ischemia/reperfusion injury.…”

Section: Discussionmentioning

confidence: 99%

miR‐376b‐3p attenuates mitochondrial fission and cardiac hypertrophy by targeting mitochondrial fission factor

Sun

Yang

et al. 2018

Clin Exp Pharma Physio

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Mitochondrial dysfunction contributes to the pathogenesis of cardiac hypertrophy. The disequilibrium of mitochondrial dynamic, which refers to mitochondrial fusion and fission, leads to mitochondrial morphology alteration and dysfunction. Enhanced understanding of the molecular mechanisms in depth may shed light on the therapy of the disease. In this study, we show that mitochondrial fission factor (MFF) is up-regulated upon hypertrophic agonist noradrenaline (NA) treatment. Knockdown of MFF attenuated NA induced mitochondrial fission and cardiac hypertrophy. Mitochondrial fission factor is a direct target of miR-376b-3p, which attenuated expression enhanced MFF expression through binding to its 3'UTR. Expression of miR-376b-3p weakened the fragmentation of mitochondria as well as decreased hypertrophic response through regulating MFF in NA treated neonatal rat ventricular cells (NRVCs). This study suggested that miR-376b-3p is a novel modulator affecting mitochondrial morphology through targeting MFF.

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“…Mitochondrial miRNAs are more speci cally targeted towards regulating pathways related to cell apoptosis, proliferation and differentiation [16]. More speci cally to processes related to mitochondrial morphogenesis, miR-200a-3p has been shown to promote mitochondrial elongation by targeting mitochondrial ssion factor (Mff) [17]. Using an anti-tumor drug, doxorubicin-induced cardiomyopathy can be counteracted using miR-532-3p, which targets mitochondrial ssion and fusion processes in cardiomyocytes [18].…”

Section: Introductionmentioning

confidence: 99%

LncRNA PVT1 Mediated by ZFP36L2 Regulates Myocardial Ischemia/Reperfusion Injury and Attenuates Mitochondrial Fusion and Fission via Activating miR-21-5p/MARCH5 Axis

Huang¹,

Tan²,

Guo³

et al. 2020

Preprint

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BackgroundAmong several leading cardiovascular disorders, ischemia-reperfusion (I/R) injury causes severe manifestations including acute heart failure, inflammation, and systemic dysfunction. Recently, there has been increasing evidence suggesting that alterations in mitochondrial morphology play a role in the prognoses of cardiac disorders. Long non-coding RNAs (lncRNAs) form major regulatory networks to modify gene transcription and translation. While several roles of lncRNAs have been explored in cancer and tumor biology, their implications on mitochondrial morphology and functions remain to be elucidated. MethodsThe functional roles of ZFP36L2 and lncRNA PVT1 were determined by a series of cardiomyocyte hypoxia/ reoxygenation (H/R) in vitro and myocardial I/R injury in vivo experiments. Quantitative Reverse transcription-polymerase chain reaction (qRT-PCR) and western blot analysis were used to detect the mRNA levels of ZFP36L2 and mitochondrial fission and fusion markers in the myocardial tissues and cardiomyocyte. Cardiac function was determined by immunohistochemistry, H&E, Masson’s staining and echocardiogram. Ultrastructural analysis of mitochondrial fission was performed using transmission electron microscopy (TEM). The mechanistic model of PVT1 with ZFP36L2 and miR-21-5p with MARCH5 was detected by subcellular fraction, RNA pull down, FISH, and luciferase reporter assays.ResultsIn this study, we report a novel regulatory axis involving lncRNA PVT1, microRNA miR-21-5p, and E3 ubiquitin ligase MARCH5, which alters mitochondrial morphology during myocardial I/R injury. Using an in vivo I/R injury mouse model and in vitro cardiomyocyte H/R model, we observed that zinc finger protein ZFP36L2 directly associated with PVT1 and altered mitochondrial fission and fusion. PVT1 also interacted with miR-21-5p and suppressed its expression and activity. Furthermore, we identified MARCH5 as a modifier of miR-21-5p, and expression of MARCH5 and its effect on mitochondrial fission and fusion were directly proportional to PVT1 expression during H/R injury. ConclusionsOur findings demonstrated that manipulation of PVT1-miR-21-5p-MARCH5-mediated mitochondrial fission and fusion via ZFP36L2 may be a novel therapeutic approach to regulate myocardial I/R injury.

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microRNA-200a-3p enhances mitochondrial elongation by targeting mitochondrial fission factor

Cited by 17 publications

References 62 publications

MicroRNAs Regulating Mitochondrial Function in Cardiac Diseases

MicroRNAs Regulating Mitochondrial Function in Cardiac Diseases

miR‐376b‐3p attenuates mitochondrial fission and cardiac hypertrophy by targeting mitochondrial fission factor

LncRNA PVT1 Mediated by ZFP36L2 Regulates Myocardial Ischemia/Reperfusion Injury and Attenuates Mitochondrial Fusion and Fission via Activating miR-21-5p/MARCH5 Axis

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