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Down-regulation of the insulin signaling pathway by SHC may correlate with congenital heart disease in Chinese populations
- Source :
- Clinical Science. 134:349-358
- Publication Year :
- 2020
- Publisher :
- Portland Press Ltd., 2020.
-
Abstract
- Background/Aims: Congenital heart disease (CHD) is one of the most common and severe congenital defects. The incidence of fetal cardiac malformation is increased in the context of maternal gestational diabetes mellitus (GDM). Therefore, we wanted to determine whether abnormalities in the insulin signaling pathway are associated with the occurrence of nonsyndromic CHD (ns-CHD). Methods: We used digital gene expression profiling (DGE) of right atrial myocardial tissue samples from eight ns-CHD patients and four controls. The genes potentially associated with CHD were validated by real-time fluorescence quantitative PCR analysis of right atrial myocardial tissues from 37 patients and 10 controls and the H9C2 cell line. Results: The results showed that the insulin signaling pathway, which is mediated by the SHC gene family, was inhibited in the ns-CHD patients. The expression levels of five genes (PTPRF, SHC4, MAP2K2, MKNK2, and ELK1) in the pathway were significantly down-regulated in the patients’ atrial tissues (P
- Subjects :
- Heart Defects, Congenital
0301 basic medicine
medicine.medical_specialty
Heart disease
Down-Regulation
Context (language use)
030204 cardiovascular system & hematology
PTPRF
03 medical and health sciences
0302 clinical medicine
Asian People
Downregulation and upregulation
Internal medicine
Animals
Cluster Analysis
Humans
Insulin
Medicine
Fetus
Heart development
business.industry
Gene Expression Profiling
Reproducibility of Results
General Medicine
medicine.disease
Rats
Gene expression profiling
Gene Ontology
030104 developmental biology
medicine.anatomical_structure
Endocrinology
Gene Expression Regulation
Shc Signaling Adaptor Proteins
business
Signal Transduction
Blood vessel
Subjects
Details
- ISSN :
- 14708736 and 01435221
- Volume :
- 134
- Database :
- OpenAIRE
- Journal :
- Clinical Science
- Accession number :
- edsair.doi.dedup.....ee6cf2db0ac9c7032f26e20c45cc4840