Nuclear Localization Leucine-Rich-Repeat Protein 1 Deficiency Protects Against Cardiac Hypertrophy by Pressure Overload

Zong, Jing; Li, Fangfang; Liang, Kaihui; Dai, Ru Ping; Zhang, Hao; Ling, Yan; Liu, Jiali; Xu, Luhong; Qian, Wenhao

doi:10.1159/000491664

Cited by 22 publications

(21 citation statements)

References 38 publications

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“…Transthoracic echocardiography and haemodynamic analysis were used for detection as previous study described. 15…”

Section: Echocardiographic and Haemodynamic Evaluationmentioning

confidence: 99%

“…Cardiac morphology and histomorphometric analysis were performed as previous study described. 15 Haematoxylin and eosin (H&E) staining was used to count cell surface area with more than 200 cells per group. Picrosirius Red (PSR) staining was used to count LV collagen volume with more than 10 fields for each heart.…”

Section: Cardiac Morphology and Histomorphometric Analysismentioning

confidence: 99%

“…Neonatal rat cardiomyocyte (NRCM) culture was performed as previous study described. 15 Cells were transfected with Ad-ZBTB20 (MOI = 50) or Ad-vehicle for 8 hours to overexpress ZBTB20. 16 Cells were treated with JNK activator anisomycin (40 ng/mL) to activate JNK1/2.…”

Section: Elisa Assaymentioning

confidence: 99%

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Zinc Finger Protein ZBTB20 protects against cardiac remodelling post‐myocardial infarction via ROS‐TNFα/ASK1/JNK pathway regulation

Yang

Xue

et al. 2020

J Cellular Molecular Medi

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This study aims to determine the efficacy of Zinc finger protein ZBTB20 in treatment of post‐infarction cardiac remodelling. For this purpose, left anterior descending (LAD) ligation was operated on mice to induce myocardial infarction (MI) with sham control group as contrast and adeno‐associated virus (AAV9) system was used to deliver ZBTB20 to mouse heart by myocardial injection with vehicle‐injected control group as contrast two weeks before MI surgery. Then four weeks after MI, vehicle‐treated mice with left ventricular (LV) remodelling underwent deterioration of cardiac function, with symptoms of hypertrophy, interstitial fibrosis, inflammation and apoptosis. The vehicle‐injected mice also showed increase of infarct size and decrease of survival rate. Meanwhile, the ZBTB20‐overexpressed mice displayed improvement after MI. Moreover, the anti‐apoptosis effect of ZBTB20 was further confirmed in H9c2 cells subjected to hypoxia in vitro. Further study suggested that ZBTB20 exerts cardioprotection by inhibiting tumour necrosis factor α/apoptosis signal‐regulating kinase 1 (ASK1)/c‐Jun N‐terminal kinase 1/2 (JNK1/2) signalling, which was confirmed by shRNA‐JNK adenoviruses transfection or a JNK activator in vitro as well as ASK1 overexpression in vivo. In summary, our data suggest that ZBTB20 could alleviate cardiac remodelling post‐MI. Thus, administration of ZBTB20 can be considered as a promising treatment strategy for heart failure post‐MI. Significance Statement: ZBTB20 could alleviate cardiac remodelling post‐MI via inhibition of ASK1/JNK1/2 signalling.

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“…Transthoracic echocardiography and haemodynamic analysis were used for detection as previous study described. 15…”

Section: Echocardiographic and Haemodynamic Evaluationmentioning

confidence: 99%

Section: Cardiac Morphology and Histomorphometric Analysismentioning

confidence: 99%

See 1 more Smart Citation

Zinc Finger Protein ZBTB20 protects against cardiac remodelling post‐myocardial infarction via ROS‐TNFα/ASK1/JNK pathway regulation

Yang

Xue

et al. 2020

J Cellular Molecular Medi

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“…PE signaling pathway plays an important role in cardiac hypertrophy, which activates a series of downstream signal events, including activation of NFAT3 nuclear translocation and activation of the three best-characterized mitogen-activated protein kinase (MAPK) subfamilies, namely p38, JNKs and ERKs [22,23]. In order to detect the effect of Sop on MAPK or NFAT3 signal pathway, we treated NRCMs with Sop at different concentrations (10 or 50 μM) for 48 h. Immunoblotting indicated that Sop had no effect on phosphorylation levels of (p38, JNK, ERK) and NFAT3 nuclear translocation (Supplementary Figure S5A,B).…”

Section: Sop Enhances the Decreased Autophagy In Pathological Cardiac Hypertrophymentioning

confidence: 99%

Sophoricoside ameliorates cardiac hypertrophy by activating AMPK/mTORC1-mediated autophagy

Gao

et al. 2020

Bioscience Reports

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Aim: The study aims to evaluate protective effects of sophoricoside (Sop) on cardiac hypertrophy. Meanwhile, The potential and significance of clinical transformation of Sop should be broadened and it should be firmly supported as an attractive drug for the treatment of pathological cardiac hypertrophy and heart failure. Methods: Using the phenylephrine (PE)-induced neonatal rat cardiomyocytes (NRCMs) hypertrophy model, the potent protection of Sop against cardiomyocytes enlargement was evaluated. The function of Sop was validated in mice received transverse aortic coarctation (TAC) or sham surgery. At one week after TAC surgery, mice were treated with Sop for the following 4 weeks, the hearts were harvested after echocardiography examination.Results: Our study revealed that Sop significantly mitigated TAC-induced heart dysfunction, cardiomyocyte hypertrophy and cardiac fibrosis. Mechanistically, Sop treatment induced a remarkable activation of AMPK/mTORC1-autophagy cascade following sustained hypertrophic stimulated. Importantly, the protective effect of Sop was largely abolished by the AMPKα inhibitor Compound C, suggesting an AMPK activation-dependent manner of Sop function on suppressing pathological cardiac hypertrophy. Conclusion: Sop ameliorates cardiac hypertrophy by activating AMPK/mTORC1-mediated autophagy. Hence, Sop might be an attractive candidate for the treatment of pathological cardiac hypertrophy and heart failure.

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“…Vol.62: e19180699, 2019 www.scielo.br/babt hypertrophy[21,22]. ERK1/2 is a group of protein kinases, which are distributed in the cytoplasm with the function of both serine and tyrosine phosphorylation.…”

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confidence: 99%

BMP4 Induces Cardiomyocyte Hypertrophy Through the Activation of ERK 1/2 Signaling Pathway in H9c2 Cells

Yuan

Tao

Deng

et al. 2019

Braz. arch. biol. technol.

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Bone morphogenetic protein-4 (BMP4) is a member of the bone morphogenetic protein family which plays an important role in bone formation, inflammation and cardiac hypertrophy. The aim of this study was to investigate the underlying molecular mechanism that BMP4-induced cardiomyocyte hypertrophy. H9c2 cells were used to measure cell surface area and protein synthesis. Western blot was used to examine hypertrophic marker brain natriuretic peptide (BNP) protein expression and phosphorylation of ERK1/2. The results exhibited that cell surface area, protein synthesis and BNP protein expression were increased with BMP4 treatment. While PD98059 inhibited these effects of BMP4. In addition, BMP4 treatment increased phosphorylation of ERK1/2 in a time-and dose-dependent manner. PD98059 treatment decreased phosphorylation of ERK1/2 that was increased by BMP4. These results suggest that BMP4 induces cardiomyocyte hypertrophy through the activation of ERK1/2 cell signaling pathway.

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Nuclear Localization Leucine-Rich-Repeat Protein 1 Deficiency Protects Against Cardiac Hypertrophy by Pressure Overload

Cited by 22 publications

References 38 publications

Zinc Finger Protein ZBTB20 protects against cardiac remodelling post‐myocardial infarction via ROS‐TNFα/ASK1/JNK pathway regulation

Zinc Finger Protein ZBTB20 protects against cardiac remodelling post‐myocardial infarction via ROS‐TNFα/ASK1/JNK pathway regulation

Sophoricoside ameliorates cardiac hypertrophy by activating AMPK/mTORC1-mediated autophagy

BMP4 Induces Cardiomyocyte Hypertrophy Through the Activation of ERK 1/2 Signaling Pathway in H9c2 Cells

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