Volume 11, Issue 2 (2020)
JMBS 2020, 11(2): 249-256 |
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1- MSc, Department of Genetics, Faculty of Biological Science, Tarbiat Modares University, Tehran, Iran.
2- PhD student, Department of Genetics, Faculty of Biological Science, Tarbiat Modares University, Tehran, Iran.
3- Professor, Department of Genetics, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran. , behmanesh@modares.ac.ir
2- PhD student, Department of Genetics, Faculty of Biological Science, Tarbiat Modares University, Tehran, Iran.
3- Professor, Department of Genetics, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran. , behmanesh@modares.ac.ir
Abstract: (3042 Views)
Abstract: Hyperglycemia is a major cause of diabetes. Hyperglycemia-induced endothelial dysfunction is generally believed to be the basis of diabetic vascular complications such as retinopathy, nephropathy and cardiovascular diseases. The most important molecules in endothelial cells that can sense elevated level of glucose and transmit signals into the cell are G protein-coupled receptors (GPCRs).
In the present study, according to bioinformatics analysis of genomic sequences between healthy and patient individuals, two G proteins GPR182 and CALCRL were selected and their expression level were examined in hyperglycemic and normal conditions in HUVEC as a model of vascular endothelial cells at different glucose concentrations and various time intervals. In addition, the effects of hyperglycemia on cell viability and cell cytotoxicity were assessed by MTT and LDH assay respectively and also morphological changes by immunohistochemistry.
Overall our data reveal a probable role for GPR182 and CALCRL in hyperglycemia-induced endothelial dysfunction. Thus, they could be developed as a potential molecular targets for the endothelial dysfunction therapy.
In the present study, according to bioinformatics analysis of genomic sequences between healthy and patient individuals, two G proteins GPR182 and CALCRL were selected and their expression level were examined in hyperglycemic and normal conditions in HUVEC as a model of vascular endothelial cells at different glucose concentrations and various time intervals. In addition, the effects of hyperglycemia on cell viability and cell cytotoxicity were assessed by MTT and LDH assay respectively and also morphological changes by immunohistochemistry.
Overall our data reveal a probable role for GPR182 and CALCRL in hyperglycemia-induced endothelial dysfunction. Thus, they could be developed as a potential molecular targets for the endothelial dysfunction therapy.
Article Type: Original Research |
Subject:
Molecular biotechnology
Received: 2020/01/21 | Accepted: 2020/03/27 | Published: 2020/06/9
Received: 2020/01/21 | Accepted: 2020/03/27 | Published: 2020/06/9
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