Disruption of the GPR35 expression accelerates the formation of foam cells in hyperglycemia

Authors
S. Z. Azarshin 1
M. A. Boroumand 2
S. Rabbani 3
M. Behmanesh 1
1 Department of Genetics, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran
2 Cardiovascular Diseases Research Institute, Tehran Heart Center, Tehran University of Medical Sciences, Tehran, Iran
3 Research Center for Advanced Technologies in Cardiovascular Medicine, Tehran Heart Center, Tehran University of Medical Sciences, Tehran, Iran
Abstract
Introduction: Diabetes is one of the most common metabolic disorders that increase the formation of vascular plaques and foam cells in the vessel wall by increasing inflammation in blood cells and arterial walls. Consequently, understanding the genes involved in this process can greatly help control the progression of vascular diseases. Methods: In this study, to investigate the response of GPCR receptor that may play a role in the process of foam cell formation and inflammation in diabetes, related RNAseq and microarray data were examined. Also, the association of candidate gene expression with the foam cell formation genes and co-regulating miRNAs, was evaluated. Results: The results showed that hyperglycemia led to inflammation and decreased GPR35 gene expression. GPR35 expression is also reduced in the blood of prediabetic and diabetic patients, and this decrease in expression is accompanied by changes in other genes involved in the process of foam cell formation. Also, three miRNAs named hsa-miR-320c, hsa-miR-183 and hsa-let-7e are co-regulators of GPR35 gene expression and CD36, OLR1, ABCG1 and ANGPTL4 genes involved in the foam cell formation. Conclusion: The present results indicate that the GPR35 gene may play a role in the process of inflammation and plaque formation in the arteries and it is possible that a decrease in the expression of the GPR35 gene will accelerate the occurrence of vascular complications of diabetes.

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Subjects

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Pathobiology Reserach
Volume 28, Issue 3
May 2025
Pages 59-68