Journal: BMC Cardiovascular Disorders

Article Title: Mycn ameliorates cardiac hypertrophy-induced heart failure in mice by mediating the USP2/JUP/Akt/β-catenin cascade

doi: 10.1186/s12872-024-03748-8

Figure Lengend Snippet: Mycn upregulation alleviates myocardial dysfunction in mice. Mice were administrated with lentiviral vectors-carried OE-Mycn or OE-NC, followed by ISO injection. A , HW/BW of mice. B , Myocardial injury of mice analyzed by HE staining. C , LVEF and LVFS or mice analyzed by echocardiographic assessment. D , Serum levels of CK, CK-MB, LDH, and cTnT in mice determined using ELISA kits. E , ROS content in the mouse heart determined using DHE staining. F - G , MDA content (F) and SOD activity (G) in the mouse heart tissue determined using ELISA kits. H , Concentrations of ANP and BNP in the mouse heart tissue determined using ELISA kits. I , Cell apoptosis in the mouse heart tissue examined using TUNEL assay. J , Mycn mRNA expression in the mouse heart tissue examined by RT-qPCR. In each group, n = 10. Differences were analyzed using the unpaired t test or the two-way ANOVA. * p < 0.05

Article Snippet: For artificial gene interference in mice, the animals were injected with lentiviral vectors-packaged gene overexpression plasmids of Mycn (OE-Mycn), USP2 (OE-USP2), gene knockdown plasmid of JUP (KD-JUP), or the negative control (NC) plasmids (OE-NC and KD-NC) (All provided by VectorBuilder Inc., Guangzhou, Guangdong, China).

Techniques: Injection, Staining, Enzyme-linked Immunosorbent Assay, Activity Assay, TUNEL Assay, Expressing, Quantitative RT-PCR

Journal: BMC Cardiovascular Disorders

Article Title: Mycn ameliorates cardiac hypertrophy-induced heart failure in mice by mediating the USP2/JUP/Akt/β-catenin cascade

doi: 10.1186/s12872-024-03748-8

Figure Lengend Snippet: Mycn activates USP2 transcription. A , USP2 predicted as a target of Mycn predicted in the hTFtarget system and the putative binding sites. B - C , mRNA (B) and protein (C) expression of USP2 in the heart tissue of mice after HCM modeling and OE-Mycn treatment examined by RT-qPCR and WB analysis, respectively. D , binding relationship between Mycn and the USP2 promoter in mouse cardiomyocytes determined by the ChIP assay. E , transcription activity of USP2 promoter in mouse cardiomyocytes transfected with OE-Mycn examined by the luciferase reporter gene assay. For animal experiments, n = 10 in each group. For cellular experiments, three biological replicates were conducted. Differences were analyzed by the unpaired t test or the one-way ANOVA. * p < 0.05. See full-length blot images in Supplementary Figure

Article Snippet: For artificial gene interference in mice, the animals were injected with lentiviral vectors-packaged gene overexpression plasmids of Mycn (OE-Mycn), USP2 (OE-USP2), gene knockdown plasmid of JUP (KD-JUP), or the negative control (NC) plasmids (OE-NC and KD-NC) (All provided by VectorBuilder Inc., Guangzhou, Guangdong, China).

Techniques: Binding Assay, Expressing, Quantitative RT-PCR, Activity Assay, Transfection, Luciferase, Reporter Gene Assay

Journal: BMC Cardiovascular Disorders

Article Title: Mycn ameliorates cardiac hypertrophy-induced heart failure in mice by mediating the USP2/JUP/Akt/β-catenin cascade

doi: 10.1186/s12872-024-03748-8

Figure Lengend Snippet: USP2 overexpression alleviates cardiac hypertrophy and dysfunction in mice. Mice were administrated with lentiviral vectors-carried OE-USP2 or OE-NC, followed by ISO injection. A , HW/BW of mice. B , Myocardial injury of mice analyzed by HE staining. C , LVEF and LVFS or mice analyzed by echocardiographic assessment. D , Serum levels of CK, CK-MB, LDH, and cTnT in mice determined using ELISA kits. E , ROS content in the mouse heart determined using DHE staining. F , SOD activity and MDA content in the mouse heart tissue determined using ELISA kits. G , Concentrations of ANP and BNP in the mouse heart tissue determined using ELISA kits. H , Cell apoptosis in the mouse heart tissue examined using TUNEL assay. I , Mycn mRNA expression in the mouse heart tissue examined by RT-qPCR. In each group, n = 10. Differences were analyzed using the unpaired t test or the two-way ANOVA. * p < 0.05

Article Snippet: For artificial gene interference in mice, the animals were injected with lentiviral vectors-packaged gene overexpression plasmids of Mycn (OE-Mycn), USP2 (OE-USP2), gene knockdown plasmid of JUP (KD-JUP), or the negative control (NC) plasmids (OE-NC and KD-NC) (All provided by VectorBuilder Inc., Guangzhou, Guangdong, China).

Techniques: Over Expression, Injection, Staining, Enzyme-linked Immunosorbent Assay, Activity Assay, TUNEL Assay, Expressing, Quantitative RT-PCR

Journal: BMC Cardiovascular Disorders

Article Title: Mycn ameliorates cardiac hypertrophy-induced heart failure in mice by mediating the USP2/JUP/Akt/β-catenin cascade

doi: 10.1186/s12872-024-03748-8

Figure Lengend Snippet: Graphical abstract. In the context of cardiac hypertrophy, Mycn ameliorates heart failure by activating transcription of USP2, which enhances the stability of JUP protein via deubiquitination modification and subsequently blocks the Akt/β-catenin pathway

Article Snippet: For artificial gene interference in mice, the animals were injected with lentiviral vectors-packaged gene overexpression plasmids of Mycn (OE-Mycn), USP2 (OE-USP2), gene knockdown plasmid of JUP (KD-JUP), or the negative control (NC) plasmids (OE-NC and KD-NC) (All provided by VectorBuilder Inc., Guangzhou, Guangdong, China).

Techniques: Modification