Method for researching ETR function and regulation and control mechanism in pregnancy-induced hypertension cells

Abstract

The invention discloses a method for researching ETR functions and regulation and control mechanisms in pregnancy-induced hypertension cells, and particularly relates to the field of medical research,and the method comprises the following steps: carrying out a clinical level research experiment, detecting and analyzing correlation between plasma ET-1 of a pregnancy-induced hypertension patient and inflammatory factors IL-1beta and IL-18, and carrying out a non-transgenic animal level research experiment. According to the invention, clinical experiments, animal experiments, cell experiments, transgenic animal experiments and experimental data arrangement are carried out; the function of ETR in the tunica media smooth muscle cells is analyzed and defined according to a comprehensive experiment result; the expression of ETR in vascular endothelial cells regulated and controlled by ET-1 under pregnancy-induced hypertension conditions can be clarified; the effect of increase of ETR expression in vascular medial smooth muscle cells in pregnancy-induced hypertension on vascular functions is clarified, and regulation of ETR expression in intimal smooth muscle cells by endothelial cells through activation of inflammasome under the condition of pregnancy-induced hypertension is studied.

Description

technical field [0001] The invention relates to the field of medical research, more specifically, the invention relates to a method for studying ETR function and regulation mechanism in pregnancy induced hypertension cells. Background technique [0002] The vascular dysfunction caused by pregnancy-induced hypertension persists in the postpartum period and may lead to an increased risk of cardiovascular disease in these women. Studies in the RUPP animal model have shown that the expression of ETR in vascular endothelial cells is decreased, and the expression of ETR in smooth muscle cells is increased. ETR in cells can promote vasodilation, and endothelin can up-regulate intracellular oxidative stress. Oxidative stress and endothelin can regulate the expression of ETR at the transcriptional and protein levels, respectively. However, the mechanism of action in pregnancy-induced hypertension still not clear. Endothelial cells and medial smooth muscle cells are closely related i...

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Problems solved by technology

[0002] The vascular dysfunction caused by pregnancy-induced hypertension persists in the postpartum period and may lead to an increased risk of cardiovascular disease in these women. Studies in the RUPP animal model have shown that the expression of ETR in vascular endothelial cells is decreased, and the expression of ETR in smooth muscle cells is increased. ETR in cells can promote vasodilation, and endothelin can up-regulate intracellular oxidative stress. Oxidative stress and endothelin can regulate the expression of ETR at the transcriptional and protein levels, respectively. However, the mechanism of action in pregnancy-induced hypertension still not clear

Endothelial cells and medial smooth muscle cells are closely related in the vessel wall. Therefore, it is feasible to study the regulation mechanism of ET-1 on the expression of ETR in endothelial cells and the mechanism of ETR expression in smooth muscle cells. None of them can investigate the mechanism of ETR downregulation in endothelial cells in PIH, nor can it clarify the role of ETR upregulation in smooth muscle cells in PIH

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