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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Bian, Ou Sun, Yingxian Zhang, Haishan Guan, Qigang Zeng, Dingyin |
| Description | Author Affiliation: Bian O ( Department of Cardiology, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning 110001, P.R. China.); Zhang H ( Department of Cardiology, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning 110001, P.R. China.); Guan Q ( Department of Cardiology, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning 110001, P.R. China.); Sun Y ( Department of Cardiology, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning 110001, P.R. China.); Zeng D ( Department of Cardiology, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning 110001, P.R. China.) |
| Abstract | Gap junction intercellular communication (GJIC) is important in mediating intercellular substance and signal transmission. Connexin (Cx)43 is a major component involved in GJIC in vascular tissue and its abnormal expression is closely associated with various vascular diseases. Insulin resistance is the central component of metabolic syndrome, and high doses of insulin can affect vascular function through multiple pathways, resulting in cardiovascular disease. However, the effects of insulin on GJIC function and connexin (Cx)43 expression in vascular smooth muscle cells (VSMCs) remain unclear. Following treatment of VSMCs with different doses of insulin, a fluorescence recovery after photobleaching (FRAP) assay was performed to evaluate GJIC function in treated VSMCs. The results showed that highdose insulin suppressed GJIC function. Western blot assays further demonstrated that highdose insulin induced the phosphorylation of Cx43 at s368 and downregulated the expression of Cx43. H2O2 release assays demonstrated that highdose insulin treatment significantly elevated the cellular H2O2 level. In addition, compared with cells treated with highdose insulin, pretreatment with catalase significantly restored the cellular GJIC function, decreased the phosphorylation level of Cx43 at s368, and enhanced Cx43 expression. In conclusion, these data indicate that highdose insulin inhibits cellular GJIC function through the oxidative stressactivated signaling pathway. This phenomenon may also constitute a potential mechanism underlying the pathogenesis of insulin resistance and its complications. |
| ISSN | 17912997 |
| e-ISSN | 17913004 |
| Journal | Molecular Medicine Reports |
| Issue Number | 1 |
| Volume Number | 12 |
| Language | English |
| Publisher | Spandidos Publications |
| Publisher Date | 2015-07-01 |
| Publisher Place | Greece |
| Access Restriction | Open |
| Subject Keyword | Cell Communication Drug Effects Gap Junctions Metabolism Insulin Pharmacology Muscle, Smooth, Vascular Animals Cells, Cultured Connexin 43 Fluorescence Recovery After Photobleaching Pathology Glucose Hydrogen Peroxide Hypoglycemic Agents Immunohistochemistry Cytology Phosphorylation Rats, Sprague-dawley Research Support, Non-u.s. Gov't Discipline Molecular Biology |
| Content Type | Text |
| Resource Type | Article |
| Subject | Genetics Biochemistry Molecular Biology Cancer Research Molecular Medicine Oncology |
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