Abstract
Human cytomegalovirus (HCMV) infection is one of the risk factors of cardiovascular disease; the most important pathological change is the change of vascular endothelial cell (VEC) function, but its mechanism is still unclear. Transforming growth factor β1 (TGF-β1) is an important cytokine associated with fibrosis; it can induce the occurrence of endothelial mesenchymal transition (EndMT) in VECs, which means endothelial cells acquire the characteristics and phenotypes of mesenchymal cells and secrete molecules associated with the deposition and remodeling of the extracellular matrix. Many in vivo and in vitro studies have shown that HCMV infection promotes the secretion and activation of TGF-β1. This study aims to observe the changes of endothelial cells after HCMV infection and EndMT occurrence induced by TGF-β1 and to explore the possible mechanism of HCMV infection in the pathogenesis of cardiovascular disease. Immunofluorescence staining, reverse transcription polymerase chain reaction (RT-PCR), enzyme-linked immunosorbent assay (ELISA), and immunoprecipitation methods were used in this study to analyze the changes in morphology and gene expression. We found that EndMT-related morphological and gene expression changes occurred in human umbilical vein endothelial cells (HUVECs) infected and uninfected with HCMV after treatment with TGF-β1. Human umbilical vein endothelial cells infected with HCMV, which are treated with TGF-β1, can activate the extracellular potential TGF-β1 by activating matrix metalloproteinase 2 (MMP-2). Our findings provide a molecular basis for the association between HCMV infection, TGF-β1 and cardiovascular disease.
Highlights
Human cytomegalovirus (HCMV) belongs to the β-her pesvirus family and is a double-stranded DNA virus
We found that endothelial mesenchymal transition (EndMT)-related morphological and gene expression changes occurred in human umbilical vein endothelial cells (HUVECs) infected and uninfected with HCMV after treatment with Transforming growth factor β1 (TGF-β1)
Human umbilical vein endothelial cells infected with HCMV, which are treated with TGF-β1, can activate the extracellular potential TGF-β1 by activating matrix metalloproteinase 2 (MMP-2)
Summary
Human cytomegalovirus (HCMV) belongs to the β-her pesvirus family and is a double-stranded DNA virus. It has been found that HCMV is associated with a variety of cardiovascular diseases such as atherosclerosis (AS), coronary heart disease and hypertension.[1,2,3,4,5,6] Human cytomegalovirus infection is related to the dysfunction of vascular endothelial cells (VECs).[7,8,9] Antiviral drugs, including ganciclovir, can reduce the risk of a heart transplant-associated AS.[10] Human cytomegalovirus infection can aggravate AS.[11,12,13,14] the mechanism of HCMV infection in cardiovascular disease is still unclear. Human cytomegalovirus (HCMV) infection is one of the risk factors of cardiovascular disease; the most important pathological change is the change of vascular endothelial cell (VEC) function, but its mechanism is still unclear. Many in vivo and in vitro studies have shown that HCMV infection promotes the secretion and activation of TGF-β1
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