ERK2 and Akt are negative regulators of insulin and Tumor Necrosis Factor-α stimulated VCAM-1 expression in rat aorta endothelial cells
| Autor: | Marc L. Goalstone, Gregory B. Pott, Mark Tsurudome, Nadia Bamfo |
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| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
medicine.medical_treatment Clinical Biochemistry Inflammation ERK2 Flow cytometry 03 medical and health sciences chemistry.chemical_compound Downregulation and upregulation TNFα medicine Insulin VCAM-1 Protein kinase B medicine.diagnostic_test business.industry Research Akt Cell Biology Transfection Atherosclerosis 030104 developmental biology chemistry RNAi Immunology Cancer research Tumor necrosis factor alpha medicine.symptom business |
| Zdroj: | Journal of Inflammation (London, England) |
| ISSN: | 1476-9255 |
| Popis: | Background Diabetes is quickly becoming the most widespread disorder in the Western world. Among the most prevalent effects of diabetes is atherosclerosis, which in turn is driven in part by inflammation. Both insulin and Tumor Necrosis Factor-alpha (TNFα) increase the presence of Vascular Cellular Adhesion Molecule-1 (VCAM-1) expression. The aim of this study is to determine the effects of downregulating Extracellular signal-Regulated Kinase-2 (ERK2) and Akt on insulin and TNFa-stimulated VCAM-1 expression. Methods Here we begin to define the relationships between ERK2 and Akt regulation of insulin and TNFα-stimulated VCAM-1 expression in Rat Arterial Endothelial Cells (RAEC) by transfecting RAEC with ERK2 and Akt RNA interference (RNAi) and then treating these cells with insulin (10 nM) or TNFα (10 ng/mL) alone or in combination. Results Western blot analyses, flow cytometry and confocal microscopy were used to determine changes in VCAM-1 expression within the above-stated parameters. Cells transfected with ERK2 or Akt RNAi plasmids increased insulin and TNFα-stimulated VCAM-1 total protein expression significantly (P |
| Databáze: | OpenAIRE |
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