To investigate whether EGR-1 could regulate ICAM-1expression in VGF, we established a mouse vein graft model in WT and Egr-1 KO mice.
To confirm the regulatory effect of Egr-1 on Icam-1 at the molecular level, we isolated endothelial cells from the veins of WT and Egr-1 KO mice and subjected them to mechanical stretch stimulation.
In this study, miR-551b-5p was found to have a potential to regulate EGR1 expression, which is a critical factor in VGF,[sup],, indicating that miR-551b-5p might be involved in the process of VGF via regulating of EGR-1 expression.
Endothelial dysfunction plays key roles in the processes of hypertension, diabetes, atherosclerosis, and many other diseases.[sup] After CABG surgery, vein grafts are stimulated by high arterial blood pressure, and endothelial cells are injured by mechanical stretch.[sup] ICAM-1 has been widely known for its effect in endothelial dysfunction.[sup] In this study, we also investigated the effect of Egr-1 in regulation of Icam-1 expression in VGF model in mice.
In conclusion, mechanical stretch increased miR-551b-5p expression, which promoted HUVECs proliferation and upregulated EGR-1 expression, thereby inducing endothelial dysfunction via upregulating of ICAM-1.
Disease progression mediated by egr-1 associated signaling in response to oxidative stress.
Moreover, we demonstrated that EA at PC6 acupoints significantly attenuated I/R-induced upregulation of Egr-1 as well as ERK1/2 activation in the myocardium.
Egr-1 is initially linked to the control of cell growth, survival, and transformation .
Consistently, in the current study, we found the I/R-induced myocardial expression of both p-ERK1/2 and Egr-1 was downregulated by EA at PC6 acupoints.
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Lu et al., "Egr-1, a master switch coordinating upregulation of divergent gene families underlying ischemic stress," Nature Medicine, vol.
Lowe, "Intracoronary delivery of DNAzymes targeting human EGR-1 reduces infarct size following myocardial ischaemia reperfusion," The Journal of Pathology, vol.