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find Keyword "Matrix metalloproteinase-9" 7 results
  • Expression of Vascular Endothelial Growth Factor and Matrix Metalloproteinase-9 in Hepatocellular Carcinoma

    ObjectiveTo investigate the relationship between the expression of vascular endothelial growth factor (VEGF) and matrix metalloproteinase9 (MMP9) and the recurrence or metastasis of hepatocellular carcinoma (HCC).MethodsThe expression of VEGF and MMP9 in 50 HCC tissues and in 30 normal liver tissues were examined by immunochemistry.ResultsThe positive rates of VEGF and MMP9 in HCC tissue were 86% and 68% respectively, and 53.3% and 33.3% respectively in normal liver tissue. The positive rates of VEGF and normal liver tissue (Plt;0.05). The correlation between expressions of MMP9 and VEGF was very significant (r=0.98,Plt;0.01). The positive rates of VEGF and MMP9 in HCC with metastasis were higher than that of HCC without metastasis.ConclusionVEGF and MMP9 are expressed cooperatively. Both of them play important role in the invasion and metastasis of HCC.

    Release date:2016-08-28 05:12 Export PDF Favorites Scan
  • The Effect of Cigarette Smoking on Expression of Matrix Metalloproteinase-9 in Airway Epithelium of Rats

    Objective To investigate the effects of smoking intensity, duration and cessation on mRNA and protein expressions of matrix metalloproteinase-9 ( MMP-9) in tracheal epitheliumof rats, and the relationship between smoking or smoking cessation and airway remodeling in chronic obstructive pulmonary disease ( COPD) . Methods Forty Wistar rats were randomly divided into 5 groups, ie. a normal control group, a long termheavy smoking group, a short termheavy smoking group, a long termlight smoking group,and a smoking cessation group which was exposed to room air for 10 weeks after long term heavy smoking.The expressions of MMP-9 mRNA and protein in tracheal epithelium of rats were detected by in situ hybridization and munohistochemistry respectively. Results ( 1) The pathological changes of emphysema were observed in the lung tissue of every smoking rat, and were most sever in the long term heavy smoking group. ( 2) Compared with the normal control group [ ( 0. 88 ±0. 88) PU, ( 2. 80 ±1. 66) PU] , the expressions of MMP-9 mRNA and proteins in tracheal epithelium were remarkable elevated in the long term heavy smoking group [ ( 22. 01 ±2. 86) PU, ( 20. 81 ±2. 46) PU] , the short term heavy smoking group [ ( 14. 94 ±3. 46) PU, ( 13. 68 ±2. 00) PU] , the long term light smoking group [ ( 6. 92 ±2. 71) PU,( 8. 84 ±1. 80) PU] and the smoking cessation group [ ( 19. 00 ±3. 36) PU, ( 14. 82 ±1. 74) PU] ( P lt;0. 01) . Compared with the long term heavy smoking group, the expressions of MMP-9 in tracheal epithelium were decreased in other three smoking groups ( P lt; 0. 05) . Conclusions Smoking could increase the expression of MMP-9 in tracheal epithelium and cause trachea damage and remodeling with intensity and duration in rats. Smoking cessation could decrease the MMP-9 expression and alleviate trachea remodeling,suggesting its role in the prevention of COPD.

    Release date:2016-09-14 11:23 Export PDF Favorites Scan
  • The Effect of Smooth Muscle Cell Transplantation on MyocardialMMP2, MMP9 and TIMP3 Content One Week after Myocardial Infarction

    Objective To evaluate the effect of smooth muscle cell transplantation on myocardial interstitial reconstruction shortly after myocardial infarction. Methods A total of 48 female Wister rats were randomly divided into two groups with the random number table, the control group (n=24) and the smooth muscle cell transplantation group (n=24). The left coronary artery was ligated to set up the myocardial infarction animal model. An amount of 05 ml phosphate buffered saline(PBS) containing 1×106 smooth muscle cells or 0.5 ml PBS without cells was injected into the injured myocardium immediately. By immunoblot and reverse transcriptionolymerase china reaction (RT-PCR), we observed the amount of protein and mRNA of matrix metalloproteinase2(MMP-2), matrix metalloproteinase-9(MMP-9) and tissue inhibitor of metalloprotease-3 (TIMP-3) in the myocardium of the rats. Results The transplanted smooth muscle cells survived well. Compared with the control group, myocardial TIMP3 mRNA (1.06±0.22 vs. 0.81±0.19, t=-2.358, P=0.033) and protein content (3.33±0.53 vs. 1.63±0.47, t=-6.802, Plt;0.001) were significantly increased in the transplantation group. Myocardial MMP-2, MMP-9 mRNA (0.49±0.12 vs. 1.16±0.18, t=8.453, Plt;0.001; 0.45±0.12 vs. 0.80±0.11, t=5.884, Plt;0.001) and protein content (3.98±1.08 vs. 6.05±0.91, t=4.139, P=0.001; 0.39±0.14 vs. 0.57±0.17, t=2.409, P=0.031) [CM(1585mm]were significantly reduced in the transplantation group compared with the control group. Conclusion transplanted smooth muscle cells can survive well in the infarction myocardium and can increase the amount of myocardial TIMP-3 mRNA and protein content and reduce myocardial MMP-2, MMP-9 mRNA and protein content, which is an effective way to prevent harmful cardiac remodeling.

    Release date:2016-08-30 06:02 Export PDF Favorites Scan
  • Relationship Between Plasma Matrix Metalloproteinase-9 and Hemorrhagic Transformation in Ischemic Stroke: A Systematic Review

    Objectives To study the relationship between matrix metalloproteinase-9 (MMP-9) and hemorrhagic transformation (HT) in ischemic stroke patients and provide evidence for the further clinical studies, thrombolytic therapy selection, and application of MMP inhibitors to clinical practice to extend the windows for thrombolytic therapy. Methods The studies on relationship between MMP-9 and hemorrhagic transformation in ischemic stroke were identified, in which HT was followed-up based on plasma level of MMP-9 or comparison of plasma level of MMP-9 was conducted based on HT or not, regardless of language of publication and type of design. MEDLINE (1966-Jan. 2006), EMBASE (1966-Apr. 2006), CNKI (1977-Feb.2006), and Wanfang database (1989-2005) were searched and the references lists of eligible studies were manually searched. Two reviewers independently evaluated the quality of studies and extracted data. The data were analyzed using the RevMan 4.2. and SPSS11.0 softwares. Results Six trials fulfilled the inclusion criteria, including 558 patients, 130 of them developed hemorrhagic transformation. The heterogeneity between studies was statistically significant; (Plt;0.0001). We didn’t pool the data of studies of plasma MMP-9 level. Most of the studies showed that the plasma MMP-9 level in HT or in a certain type of HT was higher than that in non-HT patients. The result of subgroup analysis showed that the plasma MMP-9 level was independently associated with HT, summary OR=14.45, 95%CI (4.90, 43.65). Conclusions The values of plasma MMP-9 in HT or in a certain type of HT are higher than that in non-HT. MMP-9 may independently be a risk of hemorrhagic transformation. The sample size of the included studies is small. So the conclusions need to be confirmed with further studies.

    Release date:2016-09-07 02:18 Export PDF Favorites Scan
  • Effect of Hepatocellular Carcinoma Cells Transfected with Inhibitory Kappa B Alpha on Expression of Nuclear Factor Kappa B and Matrix Metalloproteinase-9

    Objective To investigate the expression changes of nuclear factor kappa B (NF-κB) and matrix metalloproteinase-9 (MMP-9) in the cultured hepatocellular carcinoma cells 9204 (HCC9204) transfected with inhibitory kappa B alpha(IκB-α)vector. Methods After pcDNA3-IκB-α vector and pcDNA3 were transfected into HCC9204 by lipofectamine method, Western-blot and RT-PCR analysis were used to detect the expressions of NF-κB and MMP-9. Migration and invasion of tumor cells were assayed by fundus membrane invaded by them. Results  When pcDNA3-IκB-α was transfected into HCC9204, the expression of NF-κB was decreased at the protein level, and the expression of MMP-9 mRNA and the invision and metastasis ability of transfected cells were obviously decreased. Conclusion When the activity of NF-κB is inhibited, the ability of invasion and metastasis in HCC9204 cells decrease, which could be related to the decreased the expression of MMP-9.

    Release date:2016-09-08 11:49 Export PDF Favorites Scan
  • Expression of Matrix Metalloproteinase-9 and Tissue Inhibitor of Metalloproteinase-1 in Thyroid Carcinoma Tissue and Their Concentrations in Serum

    Objective To explore the protein expressions of matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of metalloproteinase-1 (TIMP-1), and to investigate their relationships between their serum concentration before operation and the infiltration and metastasis of thyroid carcinoma. Methods The protein expressions of MMP-9 and TIMP-1 in 32 cases of thyroid carcinomas, 23 cases of adjacent tissues and 30 cases of benign hyperplastic lesions were measured by using immunohistochemistry. The preoperative serum concentrations of MMP-9 and TIMP-1 in 21 cases of thyroid carcinomas and 19 cases of benign hyperplastic lesions were determined by enzyme-linked immunosorbent assay. Results The positive expression rates of MMP-9 and TIMP-1 in tumor tissues were significantly higher (75.0%,56.3%)than those in adjacent tissues and benign hyperplastic lesions (30.4%, 21.7%; 26.7%, 23.3%)  P<0.05. There were correlations between the expressions of MMP-9 and TIMP-1 and the local infiltrative degrees, lymph node metastasis and TNM stage (P<0.05). There was a negative correlation between the expression of MMP-9 and the expression of TIMP-1 (r=-0.509, P=0.003). The concentration of MMP-9 in serum of thyroid carcinoma patients was (122.60±36.20) ng/ml, whereas TIMP-1 was (59.44±38.65)  ng/ml, both of which were significantly higher compared to those of benign group (P<0.05).  In addition, there was a positive correlation between the expressions of MMP-9/TIMP-1 in the carcinoma tissues and their concentrations in serum (P<0.05).Conclusion To detection the expressions of MMP-9 and TIMP-1 in the lesion and their concentrations in the serum may not only contribute to the differential diagnosis of thyroid tumors, but may also help to predict the prognosis of the carcinoma.

    Release date:2016-09-08 11:49 Export PDF Favorites Scan
  • The Changes and Role of Endothelial Progenitor Cells in Acute Exacerbation of Chronic Obstructive Pulmonary Disease

    Objective To measure the level of circulating endothelial progenitor cells ( EPCs) in peripheral blood of patients with acute exacerbation of chronic obstructive pulmonary disease ( AECOPD) , and to explore the relationship between EPCs and severity markers of the disease and cardiovascular adverse outcome predictors.Methods Forty patients with COPD were recruited, including 27 at acute exacerbation phase and 13 with stable COPD from December 2010 to December 2011. Sixteen healthy nonsmokers were included as controls. Circulating EPCs were isolated by Ficoll density-gradient centrifugation and purified by Magnetic Activated Cell Sorting system. High-sensitivity C-reactive protein ( hsCRP) was estimated by using a latex immunoturbidimetric assay kit, and matrix metalloproteinase-9 ( MMP-9) was measured by enzymelinked immunosorbent assay ( ELISA) . Arterial blood gas analysis and echocardiograph were performed in the AECOPD patients. The correlations between circulating EPCs, lung function, and cardiovascular markers were investigated. Results Circulating EPCs were significantly lower in AECOPD and stable COPD patients compared with the healthy controls [ ( 5.1 ±2.6) ×103 /mL and ( 6.0 ±3.2) ×103 /mL vs. ( 9.0 ±4.3) × 103 /mL, Plt;0. 05] . EPCs had a weak correlation with hsCRP ( P = 0. 033) , but not with MMP-9. In the AECOPD patients, EPC counts were significantly inversely correlated with PASP ( pulmonary artery systolic pressure) and NT-proBNP ( amino-terminal pro-brain natriuretic peptide) levels, and positively with left ventricular ejection fraction. No correlations were found between EPCs and lung function, blood gas, hospital stays or smoking index. Conclusions Circulating EPCs were significantly lower in AECOPD patients compared with healthy controls, in which systemic inflammation might be involved. Decreased EPCs were correlated with cardiac dysfunction in patients with AECOPD, which may account for the increased cardiovascular risk in this population.

    Release date:2016-09-13 03:46 Export PDF Favorites Scan
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