TRPV1 Improve Endothelial Cell Proliferation, Migration And The Related Mechanism

objective: With the improvement of people’s living quality, the incidence rate of metabolic diseases such as hypertension, diabetes, coronary heart disease incidence, has been rising increasingly, the complication of which including stroke, heart failure, myocardial infarction, kidney damage and peripheral, heart, and central arterial disease threat to health seriously. The damage of endothelial cells, which are parts of blood vessel wall barrier, has been initial reason for vascular diseases. It is important to research the mechanism of endothelial cells on vascular diseases. Transient Receptor Potential Vanilloid 1(TRPV1) expressed in nerve cells and endothelial cells can be activated by capsaicin isolated form chili peppers. Activated TRPV1 causes an influx of calcium into the cells, increasing the concentration of calcium in cells. Continuous activating TRPV1 results in the endothelial cells relaxation, improving function of blood vessels. TRPV1 is associated with PI3K/AKT/e NOS signaling pathway, which is crucial pathway about cells proliferation. Therefore, we assumed that TRPV1 promotes endothelial cells proliferation, migration and improves endothelial cells function to prevent vascular disease by regulating PI3K/AKT/e NOS signaling pathway.Methods:Human Umbilical Vein Endothelial cells(HUVEC) was used as the object. Nine groups were included: Capsaicin, Capsazepine, Capsazepine and Capsaicin, LY294002, LY294002 and Capsaicin, L-NAME, L-NAME and Capsaicin and control. The expression of TRPV1 in HUVEC was detected by immunofluorescence staining; the migration of HUVEC in different groups was evaluated using a Transwell chamber; the proliferation of HUVEC in different groups was evaluated using CCK8 kit; the expressions of AKT, phosphor-AKT, e NOS, phosphor-e NOS in HUVEC in different groups were measured by western blotting.Results:1. TRPV1 was expressed in HUVEC.2. Treatment with TRPV1 agonist Capsaicin increased the HUVEC migration, which was abolished by the PI3 K inhibitor LY294002 and e NOS inhibitor L-NAME.3. Treatment with TRPV1 agonist Capsaicin increased the HUVEC proliferation, which were abolished by the PI3 K inhibitor LY294002 and e NOS inhibitor L-NAME.4. Treatment with TRPV1 agonist Capsaicin upregulated p-AKT, p-e NOS,which were abolished by the PI3 K inhibitor LY294002 and e NOS inhibitor L-NAME.Conclusion:1. TRPV1 was expressed in HUVEC.2. Activation of TRPV1 would increase HUVEC migration and proliferation.3. TRPV1 promotes endothelial cell migration, proliferation, increase endothelial repair ability, improve blood vessel function and prevent vascular disease by activating PI3K/AKT/e NOS signaling pathway.