Protective Effect of miR-204 on Doxorubicin-Induced Cardiomyocyte Injury via HMGB1

Du, Yiqin; Liu, Guanghui; Zhao, Luosha; Yao, Rui

doi:10.1155/2020/8819771

Cited by 11 publications

(9 citation statements)

References 31 publications

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“…30) In addition, Du, et al demonstrated that HMGB1 could attenuate the miR-204-medated prevention on DOX-induced cardiotoxic effects. 31) In our study, we discovered that DOX treatment increases the HMGB1 expression level. Furthermore, HMGB1 abolished the protective role of miR-409-3 p on cardiomyocytes under DOX treatment.…”

Section: Discussionmentioning

confidence: 63%

Circ_0001312 Silencing Suppresses Doxorubicin-Induced Cardiotoxicity via MiR-409-3p/HMGB1 Axis

Wang

Teng

et al. 2023

Int. Heart J.

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Doxorubicin (DOX) is a potent cytotoxic chemotherapeutic agent limited in clinical application owing to its cumulative and irreversible cardiotoxicity. Circ_0001312 is highly expressed in patients with heart failure. However, it is still unclear whether circ_0001312 plays any roles in DOX-induced cardiotoxicity.Human AC16 cardiomyocytes in functional group were stimulated with DOX. The levels of genes and proteins were detected by qRT-PCR and western blotting. The proliferation, apoptosis, as well as inflammatory and oxidative injury in cardiomyocytes were investigated. Dual-luciferase reporter, RNA immunoprecipitation, and pull-down assays were utilized to confirm the binding between miR-409-3p and circ_0001312 or HMGB1 (high-mobility group box 1). Exosomes were isolated by using the commercial kit and identified by transmission electron microscopy (TEM) and nanoparticle-tracking analysis (NTA).DOX impaired cardiomyocyte proliferation and induced apoptotic, inflammatory, and oxidative injury in cells. Furthermore, it promoted circ_0001312 expression, and the knockdown of circ_0001312 could reverse DOX-evoked cardiomyocyte injury. In terms of mechanics, circ_0001312 bound competitively to miR-409-3p to up-regulate HMGB1, which was a target of miR-409-3p. DOX decreased the miR-409-3p but increased the HMGB1 expression in cardiomyocytes. Functionally, miR-409-3p inhibition attenuated the protective action of circ_0001312 silencing on cardiomyocytes under DOX treatment. Moreover, miR-409-3p could abate DOXevoked apoptosis, and inflammation and oxidative stress in cardiomyocytes, and these effects were counteracted by HMGB1 overexpression. In addition, circ_0001312 was secreted by exosomes and could be transmitted via exosomes.Circ_0001312 reversed the cytotoxic effects mediated by DOX on cardiomyocytes via the miR-409-3p/ HMGB1 axis. Besides, it was released to the extracellular space by exosomes.

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Section: Discussionmentioning

confidence: 63%

Circ_0001312 Silencing Suppresses Doxorubicin-Induced Cardiotoxicity via MiR-409-3p/HMGB1 Axis

Wang

Teng

et al. 2023

Int. Heart J.

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“…Zhang et al found that rosuvastatin reduced the secretion of TNF-α and IFN-γ by reducing HMGB1 levels [211]. Du et al found that miR-204 levels were decreased after DOX treatment, and miR-204 overexpression targeted HMGB1 to directly reduce its levels, thus exerting a cardioprotective effect [212]. Besides, myeloid differentiation protein 1(MD-1) appears to be related to the regulation of TLR4 expression and DOXinduced myocardial inflammation.…”

Section: Hmgb1/tlr4/mapks/nf-κb Signaling Pathwaymentioning

confidence: 99%

Role of oxidative stress and inflammation-related signaling pathways in doxorubicin-induced cardiomyopathy

et al. 2023

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Doxorubicin (DOX) is a powerful and commonly used chemotherapeutic drug, used alone or in combination in a variety of cancers, while it has been found to cause serious cardiac side effects in clinical application. More and more researchers are trying to explore the molecular mechanisms of DOX-induced cardiomyopathy (DIC), in which oxidative stress and inflammation are considered to play a significant role. This review summarizes signaling pathways related to oxidative stress and inflammation in DIC and compounds that exert cardioprotective effects by acting on relevant signaling pathways, including the role of Nrf2/Keap1/ARE, Sirt1/p66Shc, Sirt1/PPAR/PGC-1α signaling pathways and NOS, NOX, Fe2+ signaling in oxidative stress, as well as the role of NLRP3/caspase-1/GSDMD, HMGB1/TLR4/MAPKs/NF-κB, mTOR/TFEB/NF-κB pathways in DOX-induced inflammation. Hence, we attempt to explain the mechanisms of DIC in terms of oxidative stress and inflammation, and to provide a theoretical basis or new idea for further drug research on reducing DIC.

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“…miRNA can play a significant role in the onset and progression of cardiovascular disease by coordinating various disease pathways. MiR-204 is a newly discovered miRNA with multiple protective effects on cardiovascular diseases [ 8 ]. It has been found that miR-204 can protect myocardial cells from ischemia/reperfusion injury by regulating apoptosis, and the serum miR-204 expression considerably reduced in patients with chronic obstructive pulmonary disease (COPD) accompanied with PAH [ 9 , 10 ].…”

Section: Introductionmentioning

confidence: 99%

Serum miR-204 and miR-451 Expression and Diagnostic Value in Patients with Pulmonary Artery Hypertension Triggered by Congenital Heart Disease

Qiao

Guan

et al. 2022

Computational and Mathematical Methods in Medicine

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Objective. To determine the level of expression and clinical importance of serum miR-204 and miR-451 in patients with pulmonary arterial hypertension caused by congenital heart disease (CHD-PAH). Methods. From July 2019 to January 2021, 114 infants with congenital heart disease (CHD) were hospitalized at Qingdao’s Fuwai Cardiovascular Hospital. They were grouped into categories: CHD (53 cases) and CHD-PAH (61 cases) based on whether they had pulmonary hypertension (PAH). In addition, 60 healthy children were selected as the control group. All children underwent routine biochemical examination, echocardiography, and pulmonary arterial pressure examination. By using an enzyme-linked immunosorbent assay (ELISA), the levels of brain natriuretic peptide (BNP) and asymmetric dimethylarginine (ADMA) in the blood were measured. Additionally, reverse transcription-polymerase chain reaction (RT-PCR) was used to determine the expression levels of miR-204 and miR-451 in peripheral blood. The correlation between miR-204, miR-451, BNP, ADMA, and mPAP was investigated using Pearson correlation analysis. Results. Consequently, the TC, BNP, and ADMA serum levels were considerably higher in the CHD and CHD-PAH groups than in the control group ( P < 0.05 ), whereas BNP and ADMA serum levels were significantly higher in the CHD-PAH group than in the CHD group ( P < 0.05 ). According to RT-PCR data, the expression levels of miR-204 and miR-451 in the peripheral blood of children in the CHD and CHD-PAH groups were significantly lower ( P < 0.05 ) when compared to the control group. The expression levels of miR-204 and miR-451 in the peripheral blood of children in the CHD-PAH group were substantially lower ( P < 0.05 ) than in the CHD group. Significantly, the findings of the ROC curve revealed that the area under the curve (AUC) of CHD-PAH diagnosed by miR-204 and miR-451 alone was 0.737 and 0.725, respectively, and the AUC of joint diagnosis was 0.840, which was greater than that of single diagnosis ( P < 0.05 ). Patients with CHD-PAH had lower levels of miR-204 and miR-451 in their blood, and this was found to be associated with BNP, ADMA, and mPAP, analyzed by Pearson correlation. Conclusions. Children with CHD-PAH can be diagnosed based on aberrant expressions of miR-204 and miR-451 in their peripheral blood serum. Moreover, CHD-PAH can be diagnosed if the combination of miR-204 and miR-451 is detected as a biomarker, which has a higher diagnostic value.

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Protective Effect of miR-204 on Doxorubicin-Induced Cardiomyocyte Injury via HMGB1

Cited by 11 publications

References 31 publications

Circ_0001312 Silencing Suppresses Doxorubicin-Induced Cardiotoxicity via MiR-409-3p/HMGB1 Axis

Circ_0001312 Silencing Suppresses Doxorubicin-Induced Cardiotoxicity via MiR-409-3p/HMGB1 Axis

Role of oxidative stress and inflammation-related signaling pathways in doxorubicin-induced cardiomyopathy

Serum miR-204 and miR-451 Expression and Diagnostic Value in Patients with Pulmonary Artery Hypertension Triggered by Congenital Heart Disease

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