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http://purl.uniprot.org/citations/25586361http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/25586361http://www.w3.org/2000/01/rdf-schema#comment"

Background

As Wnt/β-catenin/glycogen synthase kinase 3β (GSK3β) signaling has been implicated in myocardial injury and diabetic cardiomyopathy (DCM) is a major part of diabetic cardiovascular complications, we therefore investigated the alterations of Wnt/β-catenin/GSK3β signaling during the development of DCM.

Methods

The rat model of diabetes mellitus (DM) was established using a single intraperitoneal injection of streptozotocin (STZ, 60 mg/kg). The alterations of Wnt/β-catenin/GSK3β signaling were determined 4, 8, and 12 weeks following DM using Western blotting, immunohistochemistry, and quantitative real-time reverse transcriptase polymerase chain reaction. Cardiac pathology changes were evaluated using hematoxylin and eosin, Masson trichromatic, and terminal dUTP nick-end labeling staining.

Results

Histological analyses revealed that DM induced significant myocardial injury and progressive cardiomyocyte apoptosis. The protein and mRNA levels of Wnt2, β-catenin, and c-Myc were progressively increased 4, 8, and 12 weeks following DM. The expression of T-cell factor 4 and phosphorylated of GSK3β on Ser9 were progressively increased. However, the expression of the endogenous Wnt inhibitor Dickkopf-1 was increased after STZ injection and then decreased as DCM developed.

Conclusion

Wnt/β-catenin/GSK3β signaling pathway is activated in the development of DCM. Further investigation into the role of Wnt signaling during DCM will functionally find novel therapeutic target for DCM."xsd:string
http://purl.uniprot.org/citations/25586361http://purl.org/dc/terms/identifier"doi:10.1016/j.carpath.2014.12.002"xsd:string
http://purl.uniprot.org/citations/25586361http://purl.uniprot.org/core/author"Li J."xsd:string
http://purl.uniprot.org/citations/25586361http://purl.uniprot.org/core/author"Wang Y."xsd:string
http://purl.uniprot.org/citations/25586361http://purl.uniprot.org/core/author"Wang F.W."xsd:string
http://purl.uniprot.org/citations/25586361http://purl.uniprot.org/core/author"Mu Y.L."xsd:string
http://purl.uniprot.org/citations/25586361http://purl.uniprot.org/core/author"Chong Z.Z."xsd:string
http://purl.uniprot.org/citations/25586361http://purl.uniprot.org/core/author"Tian G.H."xsd:string
http://purl.uniprot.org/citations/25586361http://purl.uniprot.org/core/author"Xi X.H."xsd:string
http://purl.uniprot.org/citations/25586361http://purl.uniprot.org/core/author"Yin M.S."xsd:string
http://purl.uniprot.org/citations/25586361http://purl.uniprot.org/core/date"2015"xsd:gYear
http://purl.uniprot.org/citations/25586361http://purl.uniprot.org/core/name"Cardiovasc Pathol"xsd:string
http://purl.uniprot.org/citations/25586361http://purl.uniprot.org/core/pages"179-186"xsd:string
http://purl.uniprot.org/citations/25586361http://purl.uniprot.org/core/title"Activation of Wnt/beta-catenin/GSK3beta signaling during the development of diabetic cardiomyopathy."xsd:string
http://purl.uniprot.org/citations/25586361http://purl.uniprot.org/core/volume"24"xsd:string
http://purl.uniprot.org/citations/25586361http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/25586361
http://purl.uniprot.org/citations/25586361http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/25586361
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