Vascular endothelial cell(VEC) is a kind of simple squamous epithelium lined on the inner surface of blood vessels. VEC is an important barrier between the blood and tissue and it also plays a key role in regulating inflammation, thrombosis, endothelial cells mediated vasodilatation and endothelial regeneration. These processes should be controlled by a variety of complex mechanism which requires us to find out. With results of the researches in vascular endothelial cell function, the important roles that microRNA in vascular endothelial cell function draws more and more researchers' attention. MicroRNAs control gene expression in post-transcriptional level and affect the function of endothelial cells. This review focuses on the research progress on regulatory mechanism of microRNA to endothelial cell inflammation, thrombosis, vasodilation and endothelium regeneration.
bjective To investigate the correlation between expression of vascular endothelial growth factor(VEGF) of serum and tumor tissues and the clinical prognosis in patients with breast cancer. Methods The expressions of VEGF level of serum and tumor tissues in 44 patients with invasive duct breast cancer, 13 with benign breast diseases and 40 healthy controls. Serum VEGF level was measured by ELISA method. The protein expression of tissue VEGF, ER and C-erbB-2 were evaluated by immunohistochemistry LSAB method. Results Serum VEGF level and tissue VEGF expression in breast cancer were higher than those in benign breast diseases （P＜0.001）, and there was no significance in benign breast diseases and healthy controls （Pgt;0.05）. VEGF expression was correlated with lymph node metastasis (P＜0.01), ER and C-erbB-2 expression (P＜0.05, P＜0.01) and clinical stage （P＜0.01）. There were no statistical correlation between VEGF expression and age, tumor size (Pgt;0.05). Conclusion There is positively correlation between serum VEGF level and tissue VEGF expression, and between VEGF expression and clinic prognosis. Serum VEGF level may be one of important index of prognosis estimation in patients with breast cancer.
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.
ObjectiveTo investigate the expression of vascular endothelial growth factor （VEGF） and proliferating cell nuclear antigen (PCNA) in colorectal cancer and its relationship with metastasis and recurrence. MethodsParaffinembedded specimens from 59 patients with colorectal cancer, 16 patients with adenomas and 12 normal colonic tissues were examined and compared by SP immunohistochemical method. ResultsThe positive rate of VEGF in colorectal cancer were significantly higher than that in adenomas (P＜0.05). The positive rate of VEGF in Dukes A and B stage of colorectal cancer were significantly higher than those in Dukes C and D (P＜0.05). Expression of VEGF in postoperative recurrence group was markedly higher than that in the group with no recurrence (P＜0.05). Proliferative activity expression suggested that the poorer the differentiation, the more PCNA increased in case of lymphnode or hepatic metastasis. The PCNA showed marked difference between postoperative and nonpostoperative recurrences (P＜0.05). Conclusion The expression of VEGF and PCNA is closely related to the invasion and metastasis of tumor during the operation. The increased VEGF and high PCNA implies that there may be some potential metastasis present.
ObjectiveTo explore the relation between vascular endothelial growth factor （VEGF） and the formation of tumor thrombosis in the main trunks of portal vein (PVTT). MethodsTumor specimens were collected from 36 patients (16 patients with PVTT, the other patients without PVTT and metastasis) undergoing resection of hepatocellular carcinoma (HCC) and portal thrombectemy, PVTT specimens of 16 patients named group A1, the same patients’ with HCC named group A2, tumor specimens of the other patients named group B. In situ hybridization and immunohistochemistry were used to investigate VEGF mRNA, protein and microvessel density (MVD) on surgical specimens. The intensity was evaluated using a computer image analyzercell analysis system.ResultsVEGF mRNA expression was detected in the tumor’ cell of the specimens. The expression rates of VEGF mRNA in the group B, A2, A1 were 30%, 100%, 100% respectively, and the expression rates of VEGF mRNA in group A2 and A1 were higher than that in group B （P＜0.01）. The intensity of VEGF mRNA in group A2 （0.078 5±0.019 6） were lower than in group A1 （0.194 4±0.059 0） （P＜0.01）. VEGF protein expression was often detected in the tumor cell, vascular endothelial cell and fibroblast cells. Invasion was detected in small vein in group A2, more tumor cell colony detected in group A1. The expression rates of VEGF protein in group B, A2, A1 were same as VEGF mRNA; the intensity of VEGF protein in A1 （0.165 6± 0.034 5） was higher than in group A2 （0.108 1±0.024 3） （P＜0.01）. MVD in group B, A2, A1 was 31.9±14.4, 63.3±15.1, 116±27.6/view of 200 microscopefield, MVD in group A1 was higher than group A2 （P＜0.01）, higher in group A2 than in group B. There was a statistically significant correlation between the intensity of VEGF expression and MVD in group B,A2 and A1. ConclusionVEGF could play an important role in the invasion, metastasis of HCC and the formation of PVTT. Angiogenesis in tumor is correlated well with the progression of HCC.
Objective To be expressed human vascular endothelial growth factor (VEGF) recombinant protein in Escherichia Coli in high level. Methods VEGF was amplified from human fetal brain cDNA library, the amplified fragment was inserted into M13mP18 and confirmed to be VEGF165cDNA by restriction mapping and DNA sequencing, then it was combined with an expression vector PRL621. This recombinant plasmid overexpressed a 20kd recombinant protein in E.Coli(TG1), the protein was isolated and purifed from E.Coli, and initially renatured. Results The overexpressed recombinant protein was 35% of the total cell protein, the sequence of its first 15-N terminal amino acid was identrical to that of the human natural VEGF protein, Chorioallantoic membrane(CAM) assay showed that the rhVEGF promated new capillary vessels formation. Conclusion The genetic engineering Escherichia Coli can express human vascular endothelial growth factor in high level.
Objective To investigate the role of vascular endothelial growth factor ( VEGF) in the pathogenesis of emphysema and its relationship with tumor necrosis factor alpha ( TNF-α) . Methods 48 rats were randomly divided into four groups, ie. a normal control group, an emphysema group, a rhTNFR∶Fc intervention group, and a sham intervention group. The rats in the emphysema group, the rhTNFR: Fc intervention group, and the shamintervention group were exposed to cigarette smoking for 80 days. After 30 days of exposure, rhTNFR: Fc hypodermic injection was administered in the rhTNFR: Fc intervention group while placebo was injected in the sham intervention group as control. Lung tissue sections were stained by hematoxylin and eosin. Mean linear intercept ( MLI) and mean alveolar numbers ( MAN) were measured to estimate the extent of emphysema. The level of TNF-αin serumand BALF, and the level of VEGF in BALF were measured with ELISA. Results In the emphysema group, MLI was higher and MAN was lower than those in the normal control group. Moreover, the levels of TNF-αin serum and BALF were higher, and thelevel of VEGF in BALF was lower significantly ( P lt;0. 05) . After the intervention with rhTNFR∶Fc, MAN increased and the serum TNF-αdecreased significantly compared with the emphysema group ( P lt; 0. 05) .However there were no significant differences in MLI, VEGF, and TNF-α in BALF ( P gt; 0. 05 ) . No correlation was found between the level of TNF-αand VEGF in BALF in the emphysema group. Conclusion VEGF and TNF-αare related to the pathogenesis of emphysema of smoking rats, and may contribute to the development of emphysema in different pathways.
Objective To observe the impact of collagen patches using 1-ethyl-3- （3-dimethylaminopropyl) carbod-iimide hydrochloride chemistry （EDC） to conjugate vascular endothelial growth factor （VEGF） ＋ basic fibroblast growth factor （bFGF） or VEGF alone on the survival rate of transplanted human bone morrow mesenchymal stem cells （hBM-MSCs）in vitro and in vivo. Methods Collagen patches which were activated by EDC were used as the control group，and EDC activated collagen patches that were conjugated with VEGF or VEGF ＋ bFGF were used as the experiment groups（VEGF group and VEGF ＋ bFGF group）. hBM-MSCs （0.5×106/patch） were used as seeding cells to construct engineered heart tissue （EHT）. MTT assay was performed to assess in vitro proliferation of hBM-MSCs on 3 different collagen patches. Ventricular aneurysm model after myocardial infarction was created by left anterior descending artery （LAD） ligation in male SD rats，and EHT which were constructed with 3 different patches were used for ventricular plasty. Four weeks later，immunofluorescence staining was used to examine arteriole density （anti-α-SMA staining） and transplanted cell survival （anti-h-mitochondria staining）. Results （1） hMSCs proliferation in VEGF group and VEGF ＋ bFGF group was significantly better than that in the control group on the 2nd and 4th day after cell transplantation （P＜0.05）； （2） Four weeks afterEHT implantation，immunofluorescence staining for α-SMA revealed that arteriole density of VEGF group and VEGF ＋ bFGF group was significantly higher than that of the control group （P＜0.05）； （3） Immunofluorescence staining forh-mitochondria showed that survival rates of transplanted hBM-MSCs of VEGF group and VEGF ＋ bFGF group were significantly higher than that of the control group （P＜0.05）； （4） There was a significantly positive correlation between survival rate of hBM-MSCs and arteriole density （r 2=0.99，P=0.02）. Conclusion VEGF or VEGF ＋ bFGF conjugated collagen patch can significantly improve hBM-MSCs proliferation in vitro and enhance survival rate of transplanted hBM-MSCs by accelerating revascularization of EHT in vivo.