Objective To observe the proliferation and migration of endothelial cells after 30% total burn surface area (TBSA) of deep partial thickness scald, and the effect of basic fibroblast growth factor (bFGF) on angiogenesis during wound healing.Methods A total of 133 male Wistar ratswere divided randomly into normal control (n=7), injured control group (n=42), bFGF group (n=42) andanti-c-fos group (n=42). The apoptosis expression of fibroblasts was determinedwith in situ hybridization and the changes of proliferation cell nuclear antigen(PCNA), focal adhesion rinase(FAK), c-fos and extracellular signalregulated kinase(ERK) proteins expression were detected with immunohistochemistry staining technique after 3 hours, 6 hours, 1 day, 3 days, 7 days, 14 days and 21 days of scald.Results In injured control group and bFGF group, theproliferation rate of the vascular endothelial had evident changes 7 days and14 days after scald； the expression of FAK was increased 14 days after scald. ERK proteins expression was different between injury control group and bFGF group at initial stage after scald. Stimulation of ERKs by bFGF led to up-regulation of c-fos and b expression of FAK. Conclusion Exogenous bFGF extended the influence on wound healing process by ERK signaling pathway, affecting migration cascade of vascular endothelial cell. The oncogene proteins play an important role on accelerating angiogenesis duringwound healing.
ObjectiveTo summarize the progress on the injury mechanism of vascular endothelial cells in atherosclerosis.MethodsThe latest progress was reviewed in recent literatures.ResultsAll kinds of etiological factors have activated NF-kappa B and cytokines in the development of atherosclerosis, which lead to expression of cell adhesive molecules and adhesion of monocytes to vascular endothelial cells.A variety of inflammatory mediums are released, which can directly damage endothelial cells.Besides, the inflammatory mediums make monocytes and neutrophils attach to endothelial cells by immune mechanisms, which injure the endothelial cells more severely. Meanwhile the damaged membrance structure leads to the production of AECA which activates the complementary system. Then the vascular endothelial cell injury is aggravated and the development of atherosclerosis accelerated. ConclusionIt is very important to recognize the injury mechanism of vascular endothelial cells in the development of atherosclerosis for prevention and treatment of atherosclerosis.
Objective To compare the effects of flap delay and vascular endothelial growth factor (VEGF) on the viability of the rat dorsal flap. Methods Thirty rats were divided into 3 groups: saline group, flap delay group and VEGF group. The rats in flap delay group underwent flap delay by keeping bipedicle untouched, and the cranial pedicle was cut 7 days later. The rats in VEGF group were given VEGF solution locally when the flaps were elevated in the operation. The ratsin saline group were given saline solution in the same way. Five days after thesingle pedicle flaps were performed, the flap survival rate was measured. Theflap tissues were collected to measure and analyze the microvascular density, diameter and sectional area by immunochemical method. Results The flap survival rate of flap delay group was similar to that of VEGF group andthere is no statistically significant difference(Pgt;0.05). The vascular diameter of flap delay group was much larger than that of saline group and VEGF group, showing statistically significant difference (Plt;0.05). The vascular density of VEGF group was much higher than that of saline group and flap delay group, showing statistically significant difference (Plt;0.05). The vascular sectional area of flap delay group was similar to that of VEGF group(Pgt;0.05). Conclusion The change in the flap after flap delayis manifested as obvious dilatation of microvessels, while the change in the flap after the injection of VEGF is manifested as obvious vascular proliferation. Both flap delay and VEGF can increase the vascular sectional area and the viability of the flap, but the mechanism is different.
Objective To study the effect of vascular endothelial cell growth factor (VEGF) on repair of bone defect with cortical bone allograft. Methods Forty five New Zealand white rabbits, weighted 2.5-3.0 kg, were made bone defect model of 1.5 cm in length in the bilateral radii and then were randomly divided into 3groups. The defect was repaired with only cortical bone allograft in the control group, with the cortical bone allograft and local injection of human recombinantVEGF in the experimental group, and with the cortical bone allograft and abdominal injection of VEGF PAb3 in the antagonist group. Roentgenography, immunohistochemical staining and tetracycline labelling were carried out to evaluate the reparative results 1, 3, 5, 8 and 16 weeks after operation. Results Immunohistochemical staining results showed that a great deal of blood vessels formed in the experimental group, and the number of blood vessels increased gradually with the time and reached the highest value at the 8th week. Tetracyclinelabelling showed the same result.The best results in callus formation, ossification rate and count of microvascular density were shown in the experimental group, while those in the control group were significantly better than those in the antagonist group (Plt;0.05),but there was no significant difference between the experimental group and the control group at the 8th week and the 16th week (Pgt;0.05). Conclusion VEGF can accelerates the bone formation and angiogenesis in the bone allografts, thus it can promote the repair of bone defects.
In order to study the effect of vascular endothelial cell growth factor (VEGF) on the survival of skin flap 30 SD rats were used. A randomized flap measuring 7.5 cm x 3.0 cm was created on the back of each SD rat. The treatment group (n = 10) received VEGF 40 ng/flap by subcutaneous injection with microinjector during and 24 hours after operation. The control groups received heparin 16 U/flap (n = 10) or normal saline 800 microliters/flap (n = 10). After operation, on the 3rd and 11th day, the survival rate of the skin flaps and the dermovascular density of each flap were investigated by histological and histo-morphometrical examination. The results showed that there was no significant difference in the survival rate between the treatment group and the controls on the 3rd day after operation, while on the 11th day, there was a significant difference between them, and the survival rate was much higher in the treatment group. Besides, dermovascular density was much more increased in the treatment group than that in the controls, especially in the distal 1/3 of the flap (P lt; 0.02). The conclusion was that VEGF could .
Objective To observe the effects of Galectin-3 on proliferation of vascular endothelial cells derived from peripheral blood endothelial progenitor cells. Methods The cultured peripheral blood endothelial progenitor cells in vitro were isolated and purified from human peripheral blood, and the cells were differentiated into vascular endothelial cells. Then the cells were cultivated with the galectin-3 of different concentrations, and to observe the proliferation of endothelial cells derived from peripheral blood endothelial progenitor cells. Results The abilities of proliferation of endothelial cells derived from peripheral blood endothelial progenitor cells of 0.1, 1.0, 2.5, 5.0, and 10.0 μg/ml groups were higher than that of 0 μg/ml group, there were not statistic significance of the differences between the 0.1，1.0, 2.5, and 0 μg/ml groups （P＞0.05）. But the abilities of proliferation of 5.0 and 10.0 μg/ml groups were obviously higher than that of 0, 0.1, 1.0, and 2.5 μg/ml groups （P＜0.05）, and the abilities of proliferation of 10.0 μg/ml group was also higher than that of 5.0 μg/ml group （P＜0.05）. Conclusion Galectin-3 can promote the proliferation of endothelial cells derived from peripheral blood endothelial progenitor cell.
Abstract: Objective To study the expression of E-selectin on vascular endothelial cells of nude mice liver induced by esophageal carcinoma cells, in order to find out the function of E-selectin in the metastasis of esophageal carcinoma into the liver. Methods Twelve Balb/c nude mice aged from 6 to 8 weeks with their weight ranged between 20 and 25 grams were selected in our research. The mice were equally distributed into the experimental group and the control group(n=6). EC9706 cell solution (5×10.6/0.02 ml) were injected beneath the splenic capsule of the mice in the experimental group. One hour later, spleen was removed. For the mice in the control group, after laparotomy, phosphate buffer without EC 9706 was injected beneath the splenic capsule and spleen was also removed one hour after the injection. Eight hour later, we resected the liver of the nude mice, and expression of E-selectin on vascular endothelial cells of the liver was detected with reverse transcription polymerase chain reaction (RT-PCR) and immunohistochemistry (IHC). Results In the experimental group, 8 hours after injection of EC9706 cells (5×10.6), the results of RT-PCR showed expression of E-selectin mRNA in the liver, and IHC showed a positive protein expression of E-selectin in the cytosol and membrane of hepatic sinus vessels.However, no E-selectin mRNA expression was found in the control group and IHC showed a negative protein expression of E-selectin. Conclusion Human esophageal carcinoma cell line EC9706 can induce balb/c mice liver vascular endothelial cell E-selectin expression, which shows that EC9706 may stay in the liver and form etastatic focus.
Objective To investigate the role of vascular endothelial growth factor-C (VEGF-C) and its receptors in the formation of lymphatic vessels and lymphatic metastasis in gastric cancer. Methods By the domestic and overseas literatures review, the expressions of VEGF-C and its receptors in gastric cancer, their role in tumor lymphatic metastasis and prospect in treatment of gastric cancer were summarized.Results There was a significant correlation between VEGF-C and its receptors and the formation of lymphatic vessels and lymphatic metastasis in gastric cancer. VEGF-C high expression might be an early event in lymphatic metastasis and could be considered as an independent predictive factor of lymphaticmicrometastasis. By inhibition of gastric cancer cell from secrete VEGF-C or blockage of the interaction of VEGF-C with VEGFR3, it was possible to inhibit tumor angiogenesis and the invasion and distant spread of cancer cells, thereby decreased mortality and improve survival. ConclusionVEGF-C and its receptors may promote the formation of lymphatic vessels and lymphatic metastasis in gastric cancer. It may be an effective way to gastric cancer for the treatments against VEGF-C and its receptors.
Objective To explore the effects of Zhaoke defibrase and anti alpha;vbeta;3mAb (23C6) on the adhesion and immigration of bovine retinal vascular endothelial cells. Methods The culture dishes coated with vitronectin (Vn) and collagen，assays of adhesion and immigration were performed 60 minutes after different concentration of Zhaoke defibrase and anti-alpha;vbeta;3 mAb was added to the bovine retinal vascular endothelial cells. The apoptosis of bovine retinal vascular endothelial cells induced by Zhaoke defibrase and anti-alpha;vbeta;3 mAb was detected by electron microscopy. Results Both Zhaoke defibrase and anti-alpha;vbeta;3 mAb inhibited the adhesion and immigration of bovine retinal vascular endothelial cells in a dose-dependent manner. The inhibited concentration (IC50) of Zhaoke defibrase was less than 0.05 mu;mol/L, while (IC50) of anti-alpha;vbeta;3 mAb was more than 2.5 mu;mol/L. 81.8% endothelial cells adhering to Vn were inhibited by 0.1 mu;mol/L Zhaoke defibrase, while 76.3% by endothelial cells adhering to Vn were inhibited by 10 mu;mol/L anti-alpha;vbeta;3 mAb. Typical apoptosis cells were found in bovine retinal vascular endothelial cells after affected by Zhaoke defibrase and anti-alpha;vbeta;3 mAb. Conclusion Both Zhaoke defibrase and anti- alpha;vbeta;3mAb can significantly inhibit the adhesion and immigration of bovine retinal vascular endothelial cells to extracellular matrix， and the mechanism may lie in inducing the apoptosis of endothelial cells. (Chin J Ocul Fundus Dis, 2005,21:118-121)
Objective To study the differenation of adult marrow mesenchymal stem cells(MSCs) into vascular endothelial cells in vitro and to explore inducing conditions. Methods MSCs were isolated from adult marrow mononuclear cells by attaching growth. MSCs were divided into 4 groups to induce: the cells seeded at a density of 5×103/cm2 in 2% and 15% FCS LDMEM respectively (group1 and group 2)， at a density of 5×104/cm2 in 2% and 15% FCS LDMEM respectively (group 3 and group 4); vascular endothelial growth factor(VEGF) supplemented with Bovine pituitary extract was used to induce the cell differentiation. The differentiated cells were identified by measuring surfacemarks (CD34, VEGFR2, CD31 and vWF ) on the 14th day and 21st day and performed angiogenesis in vitroon the 21st day.The cell proliferation index（PI）of different inducing conditions were measured. Results After induced in VEGF supplemented with Bovine pituitary extract, the cells of group 3 expressed the surface marks CD34, VEGFR-2, CD31 and vWF on the 14th day, the positive rates were 8.5%, 12.0%, 40.0% and 30.0% respectively, and on the 21st day the positive ratesof CD34 and VEGFR2 increased to 15.5％ and 20.0％, while the other groups did not express these marks; the induced cells of group 3 showed low proliferating state(PI was 10.4%) and formed capillary-like structure in semisolid medium. Conclusion Adult MSCs can differentiate into vascular endothelial cellsafter induced by VEGF and Bovine pituitary extract at high cell densities and low proliferatingconditions，suggesting that adult MSCs will be ideal seed cells forthe therapeutic neovascularization and tissue engineering.