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http://purl.uniprot.org/citations/24296617http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/24296617http://www.w3.org/2000/01/rdf-schema#comment"

Objectives

The present study was designed to decipher the molecular mechanisms underlying angiotensin (Ang) II-induced overexpression of connective tissue growth factor (CTGF) in cultured cardiomyocytes.

Methods

Cardiomyocytes isolated from 1-to 3-day-old neonatal rats were cultured and treated with 100 nM Ang II with or without pretreatment with 10 nM telmisartan, an Ang II type 1 receptor antagonist. The role of microRNA (miR)-19b in the regulation of Ang II-induced CTGF expression was evaluated in cultured cardiomyocytes with quantitative real-time reverse transcription polymerase chain reaction and Western blot analysis.

Results

We provide several lines of evidence to show that miR-19b contributes to the Ang II-induced overexpression of CTGF in cultured cardiomyocytes. Firstly, administration of Ang II decreased the level of miR-19b dramatically (p < 0.05 vs. control), which was abolished by telmisartan. Secondly, Ang II increased the level of CTGF significantly (p < 0.05 vs. control), which was also prevented by pretreatment with telmisartan. Thirdly, overexpression of miR-19b decreased CTGF levels (p < 0.05 vs. control). Finally, transfection of miR-19b into cardiomyocytes prevented the upregulation of CTGF induced by Ang II.

Conclusion

Downregulation of miR-19b contributes to Ang II-induced overexpression of CTGF in cultured cardiomyocytes."xsd:string
http://purl.uniprot.org/citations/24296617http://purl.org/dc/terms/identifier"doi:10.1159/000355429"xsd:string
http://purl.uniprot.org/citations/24296617http://purl.uniprot.org/core/author"Gao S."xsd:string
http://purl.uniprot.org/citations/24296617http://purl.uniprot.org/core/author"Wang Z."xsd:string
http://purl.uniprot.org/citations/24296617http://purl.uniprot.org/core/author"Cai J."xsd:string
http://purl.uniprot.org/citations/24296617http://purl.uniprot.org/core/author"Liu T.W."xsd:string
http://purl.uniprot.org/citations/24296617http://purl.uniprot.org/core/author"Yang X.C."xsd:string
http://purl.uniprot.org/citations/24296617http://purl.uniprot.org/core/author"Chi H.J."xsd:string
http://purl.uniprot.org/citations/24296617http://purl.uniprot.org/core/author"Jiao Z.Y."xsd:string
http://purl.uniprot.org/citations/24296617http://purl.uniprot.org/core/date"2014"xsd:gYear
http://purl.uniprot.org/citations/24296617http://purl.uniprot.org/core/name"Cardiology"xsd:string
http://purl.uniprot.org/citations/24296617http://purl.uniprot.org/core/pages"114-120"xsd:string
http://purl.uniprot.org/citations/24296617http://purl.uniprot.org/core/title"Downregulation of microRNA-19b contributes to angiotensin II-induced overexpression of connective tissue growth factor in cardiomyocytes."xsd:string
http://purl.uniprot.org/citations/24296617http://purl.uniprot.org/core/volume"127"xsd:string
http://purl.uniprot.org/citations/24296617http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/24296617
http://purl.uniprot.org/citations/24296617http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/24296617
http://purl.uniprot.org/uniprot/P01019#attribution-BF3366913D12AAB08E64E65C6CDEBA11http://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/24296617