Hui-Qiang Gao1, Shang-Dong Xu1, Jiang-Rong Li1, Jun Zheng1, Li-Zhong Sun2. 1. Department of Cardiovascular Surgery, Beijing Anzhen Hospital, Capital Medical University, Beijing Institute of Heart, Lung and Blood Vessel Diseases, and Beijing Engineering Research Center of Vascular Prostheses, Beijing, China. 2. Department of Cardiovascular Surgery, Beijing Anzhen Hospital, Capital Medical University, Beijing Institute of Heart, Lung and Blood Vessel Diseases, and Beijing Engineering Research Center of Vascular Prostheses, Beijing, China. Electronic address: lizhongsun@foxmail.com.
Abstract
BACKGROUND: In the design and development of small-caliber artificial blood vessels, endothelialization is a key issue, but it is not well understood at present. Some studies have used vascular endothelial growth factor (VEGF) sustained-release methods to promote endothelial cell proliferation. However, this method is not ideal. This study has used drugs to induce endothelial cells to produce VEGF. This method in turn functions to promote cell proliferation and promote the endothelialization of artificial blood vessels. This study aimed to investigate the effect of the antiplatelet drug tirofiban on endothelial cell proliferation in vitro. METHODS: In this study, human umbilical vein endothelial cells (HUVECs) were used to determine the effect of tirofiban-stimulated cell proliferation. Analysis of cell proliferation, assayed by the Cell Counting Kit-8 assay, showed that the number of cells was increasingly higher than in the absence of tirofiban. It was also observed that heparin enhanced the tirofiban effect. The cell VEGF expression at different time points after tirofiban addition was detected by western blot analysis. RESULTS: The absorbance values of the experimental (1 μg/mL tirofiban) and the control groups (0 tirofiban) were 1.74 (SD, 0.03) and 1.51 (SD, 0.07) (P < .001), respectively, after 4 days of culture under the same conditions. The amount of VEGF produced by HUVECs gradually increased after treatment with tirofiban, reached a peak at 2 hours, and was 1.3-fold greater than the control group (P = .034). Compared with the tirofiban-only group, the absorbance value of the tirofiban and 10 μg/mL of heparin group was significantly increased (P < .001). CONCLUSIONS: Tirofiban promoted the proliferation of HUVECs by promoting the synthesis of VEGF in HUVECs. Heparin enhanced tirofiban activity in promoting HUVEC proliferation.
BACKGROUND: In the design and development of small-caliber artificial blood vessels, endothelialization is a key issue, but it is not well understood at present. Some studies have used vascular endothelial growth factor (VEGF) sustained-release methods to promote endothelial cell proliferation. However, this method is not ideal. This study has used drugs to induce endothelial cells to produce VEGF. This method in turn functions to promote cell proliferation and promote the endothelialization of artificial blood vessels. This study aimed to investigate the effect of the antiplatelet drug tirofiban on endothelial cell proliferation in vitro. METHODS: In this study, humanumbilical vein endothelial cells (HUVECs) were used to determine the effect of tirofiban-stimulated cell proliferation. Analysis of cell proliferation, assayed by the Cell Counting Kit-8 assay, showed that the number of cells was increasingly higher than in the absence of tirofiban. It was also observed that heparin enhanced the tirofiban effect. The cell VEGF expression at different time points after tirofiban addition was detected by western blot analysis. RESULTS: The absorbance values of the experimental (1 μg/mL tirofiban) and the control groups (0 tirofiban) were 1.74 (SD, 0.03) and 1.51 (SD, 0.07) (P < .001), respectively, after 4 days of culture under the same conditions. The amount of VEGF produced by HUVECs gradually increased after treatment with tirofiban, reached a peak at 2 hours, and was 1.3-fold greater than the control group (P = .034). Compared with the tirofiban-only group, the absorbance value of the tirofiban and 10 μg/mL of heparin group was significantly increased (P < .001). CONCLUSIONS:Tirofiban promoted the proliferation of HUVECs by promoting the synthesis of VEGF in HUVECs. Heparin enhanced tirofiban activity in promoting HUVEC proliferation.
Authors: S de Frutos; M Griera; M Hatem-Vaquero; S Campillo; E Gutiérrez-Calabres; D García-Ayuso; M Pardo; L Calleros; M Rodríguez-Puyol; D Rodríguez-Puyol Journal: Cell Biosci Date: 2022-01-28 Impact factor: 7.133