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http://purl.uniprot.org/citations/33520084http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/33520084http://www.w3.org/2000/01/rdf-schema#comment"

Purpose

Studies have found that microRNAs (miRNAs) are closely associated with atrial fibrillation, but their specific mechanism remains unclear. The purpose of this experiment is to explore the function of miR-29b-3p in regulating atrial remodeling by targeting PDGF-B signaling pathway and thereby also explore the potential mechanisms.

Methods

We randomly divided twenty-four rats into four groups. Caudal intravenous injections of angiotensin-II (Ang-II) were administered to establish atrial fibrosis models. Expressions of miR-29b-3p and PDGF-B were then tested via RT-PCR, western blot, and immunohistochemistry. Binding sites were then analyzed via the bioinformatics online software TargetScan and verified by Luciferase Reporter. We used Masson staining to detect the degree of atrial fibrosis, while immunofluorescence and western blot were used to detect the expressions of Collagen-I and a-SMA. We used immunohistochemistry and western blot to detect the expression of connexin 43 (Cx43).

Results

In comparison with the Ang-II group, miR-29b-3p was seen to lower the degree of atrial fibrosis, decrease the expression of fibrosis markers such as Collagen-I and a-SMA, and increase the protein expression of Cx43. MiR-29b-3p can lower the expression of PDGF-B, while the Luciferase Reporter showed that PDGF-B is the verified target gene of miR-29b-3p.

Conclusions

MiR-29b-3p was able to reduce atrial structural and electrical remodeling in the study's rat fibrosis model. This biological function may be expressed through the targeted regulation of the PDGF-B signaling pathway."xsd:string
http://purl.uniprot.org/citations/33520084http://purl.org/dc/terms/identifier"doi:10.1155/2021/3763529"xsd:string
http://purl.uniprot.org/citations/33520084http://purl.uniprot.org/core/author"Hu Y."xsd:string
http://purl.uniprot.org/citations/33520084http://purl.uniprot.org/core/author"Xu T."xsd:string
http://purl.uniprot.org/citations/33520084http://purl.uniprot.org/core/author"Lu P."xsd:string
http://purl.uniprot.org/citations/33520084http://purl.uniprot.org/core/author"Lv X."xsd:string
http://purl.uniprot.org/citations/33520084http://purl.uniprot.org/core/date"2021"xsd:gYear
http://purl.uniprot.org/citations/33520084http://purl.uniprot.org/core/name"Oxid Med Cell Longev"xsd:string
http://purl.uniprot.org/citations/33520084http://purl.uniprot.org/core/pages"3763529"xsd:string
http://purl.uniprot.org/citations/33520084http://purl.uniprot.org/core/title"Overexpression of MiR-29b-3p Inhibits Atrial Remodeling in Rats by Targeting PDGF-B Signaling Pathway."xsd:string
http://purl.uniprot.org/citations/33520084http://purl.uniprot.org/core/volume"2021"xsd:string
http://purl.uniprot.org/citations/33520084http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/33520084
http://purl.uniprot.org/citations/33520084http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/33520084
http://purl.uniprot.org/uniprot/#_A0A221LG85-mappedCitation-33520084http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/33520084
http://purl.uniprot.org/uniprot/#_Q63740-mappedCitation-33520084http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/33520084
http://purl.uniprot.org/uniprot/#_Q05028-mappedCitation-33520084http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/33520084
http://purl.uniprot.org/uniprot/Q63740http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/33520084
http://purl.uniprot.org/uniprot/A0A221LG85http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/33520084
http://purl.uniprot.org/uniprot/Q05028http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/33520084