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http://purl.uniprot.org/citations/26861724http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/26861724http://www.w3.org/2000/01/rdf-schema#comment"

Introduction

MicroRNA-208a (miR-208a) exacerbated cardiomyocyte apoptosis via inhibiting nemo-like kinase (NLK). miR-208a is a crucial molecule in the regulation of heart diseases, however, the biological function and underlying mechanism of miR-208a in the progression of cardiomyocyte apoptosis is not clearly elucidated. We hypothesized that miR-208a might potentiate cardiomyocyte apoptosis through inhibiting NLK.

Methods

Male Sprague-Dawley rats were underwent permanent coronary artery ligation to establish myocardial infarction (MI) model. The quantitative real-time RT-PCR (qRT-PCR) was used to evaluate the expression of miR-208a and NLK mRNA. Western blot was applied to detect NLK and Bcl-2 proteins expression. Luciferase reporter assay was performed to indentify NLK as a target of miR-208a. The apoptosis of H9C2 cells was assessed by flow cytometry (FCM).

Results

miR-208a was upregulated accompanying with a significant decrease of NLK in response to MI, and stronger miR-208a staining was detected by in situ hybridization in the cytoplasm of cardiomyocytes in MI group compared to the sham group. In vitro, overexpression of miR-208a greatly enhance Ang II-induced the apoptosis of H9C2 cells through downregulating of NLK and the anti-apoptosis protein Bcl-2 expression, whereas these effects were reversed when miR-208a was downregulated. Dual luciferase reporter assay and western blot results demonstrated that NLK was a direct target of miR-208a. Interestingly, upregulation of NLK obviously increased Bcl-2 expression and reduced the percentage of apoptotic cells, while attenuation of NLK reduced the level of Bcl-2 and cells apoptosis after treatment with Ang II.

Conclusions

miR-208a can promote Ang II-induced cardiomyocyte apoptosis via negatively regulating NLK expression, and inhibition of miR-208a may provide a novel therapeutic target for cardiomyocyte apoptosis."xsd:string
http://purl.uniprot.org/citations/26861724http://purl.org/dc/terms/identifier"doi:10.2174/1381612822666160210143047"xsd:string
http://purl.uniprot.org/citations/26861724http://purl.uniprot.org/core/author"Huang Y."xsd:string
http://purl.uniprot.org/citations/26861724http://purl.uniprot.org/core/author"He Y."xsd:string
http://purl.uniprot.org/citations/26861724http://purl.uniprot.org/core/author"Li J."xsd:string
http://purl.uniprot.org/citations/26861724http://purl.uniprot.org/core/author"Huang C."xsd:string
http://purl.uniprot.org/citations/26861724http://purl.uniprot.org/core/author"Yang Y."xsd:string
http://purl.uniprot.org/citations/26861724http://purl.uniprot.org/core/author"Meng X."xsd:string
http://purl.uniprot.org/citations/26861724http://purl.uniprot.org/core/date"2016"xsd:gYear
http://purl.uniprot.org/citations/26861724http://purl.uniprot.org/core/name"Curr Pharm Des"xsd:string
http://purl.uniprot.org/citations/26861724http://purl.uniprot.org/core/pages"4868-4875"xsd:string
http://purl.uniprot.org/citations/26861724http://purl.uniprot.org/core/title"MicroRNA-208a Potentiates Angiotensin II-triggered Cardiac Myoblasts Apoptosis via Inhibiting Nemo-like Kinase (NLK)."xsd:string
http://purl.uniprot.org/citations/26861724http://purl.uniprot.org/core/volume"22"xsd:string
http://purl.uniprot.org/citations/26861724http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/26861724
http://purl.uniprot.org/citations/26861724http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/26861724
http://purl.uniprot.org/uniprot/#_D3ZSZ3-mappedCitation-26861724http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/26861724
http://purl.uniprot.org/uniprot/D3ZSZ3http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/26861724