Abstract
BackgroundCoronary artery disease (CAD) is a common cardiovascular disease, and abnormal blood lipid metabolism is an important risk factor. Transforming growth factor-ß (TGF-ß) and its receptor (TGF-ßR) can inhibit the release of inflammatory factors through the SMAD pathway-mediated immune response, thereby suppressing the progression of CAD. Endoglin (TGF-ßRIII), a TGF-ßR family homologous receptor protein, is directly involved in the immunoregulatory process, but the exact mechanism is unclear. This study aimed to clarify the pathophysiological effects of endoglin on the development of atherosclerosis and to explore the mechanism of the signalling pathway.MethodsWe downloaded the GEO dataset to perform a functional analysis of SMAD family activity and TGF-ß receptor protein expression in the monocyte expression profiles of patients with familial hyperlipidaemia (FH). The effect of endoglin on endothelial cell proliferation, migration, and apoptosis was examined by disrupting the endoglin gene in human umbilical vein endothelial cells (HUVECs) and validated by western blotting. The related genes and pathways regulated by endoglin were obtained by analysing the sequencing data.ResultsResearch has shown that interference with endoglin can promote the proliferation and migration and significantly inhibit the apoptosis of vascular endothelial cells. Interference with endoglin particularly encourages the expression of VEGFB in vascular endothelial cells.ConclusionThe endoglin gene in vascular endothelial cells regulates the PI3K-Akt, Wnt, TNF, and cellular metabolism pathways by activating the SMAD pathway. RAB26, MR1, CCL2, SLC29A4, IBTK, VEGFB, and GOLGA8B play critical roles. Endoglin interacts closely with 11 proteins such as CCL2 and SEPRINE1, which participate in the vital pathway of plaque formation. Interference with endoglin can alter the course of coronary atherosclerosis.
Highlights
Coronary artery disease (CAD) is a common cardiovascular disease, and abnormal blood lipid metabolism is an important risk factor
Endoglin gene interference and subsequent experiments in normal endothelial cells As shown in Fig. 2a, the results of real-time PCR showed that the expression of endoglin in the siRNA group was significantly lower than that in the NC group (P < 0.05), which could be used for subsequent validation experiments
The results showed that interference with the endoglin gene could promote the migration of human umbilical vein endothelial cells (HUVECs) (Fig. 2c)
Summary
Coronary artery disease (CAD) is a common cardiovascular disease, and abnormal blood lipid metabolism is an important risk factor. Transforming growth factor-ß (TGF-ß) and its receptor (TGF-ßR) can inhibit the release of inflammatory factors through the SMAD pathway-mediated immune response, thereby suppressing the progression of CAD. Coronary artery disease (CAD) is a common cardiovascular disease, and abnormal lipid metabolism is an important risk factor. Transforming growth factor-ß (TGF-ß) and its receptor (TGF-ßR) inhibit the release of inflammatory cytokines through the SMAD2/3/4-mediated immune response, thereby inhibiting the progression of coronary atherosclerosis [3, 4]. In the hyperlipidaemia mouse model, soluble endoglin was significantly downregulated by statin therapy, but its expression on the aorta was significantly increased [6, 9] It remains unclear among the current academic community whether the protective effect of endoglin is a biological target for atherosclerosis. Given the importance of endoglin in the progression of coronary atherosclerosis [10, 11], its immunological properties in the course of the disease provide an excellent entry point for studying the immunological mechanisms of coronary atherosclerosis
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