Objective To explore the expressions of E-cadherin， matrix metalloproteinases-2 （MMP-2） protein，and matrix metalloproteinases-9 （MMP-9） protein in gastric cancer tissues， and to analyze the possible statistical relati-onship between the expressions of E-cadherin， MMP-2 protein， and MMP-9 protein， and clinicopathological features ofgastric cancer. Methods The ABC immunohistochemical staining was adopted to examine the expressions of E-cadherin，MMP-2 protein， and MMP-9 protein in 40 paraffin slices of gastric cancer （gastric cancer group）， with the adjacent tissue as the control group （adjacent tissue group）. The positive rates of 3 kinds of protein were compared between the2 groups， in addition， the statistical relationship between the expressions of the 3 kinds of protein and clinicopathological features of gastric cancer was examined respectively by SPSS 19.0 software. Results The expressions of E-cadherin， MMP-2 protein， and MMP-9 protein were all found in gastric cancer tissues and adjacent tissues. In gastric cancer tissue group， the expression of E-cadherin downregulated while the expressions of MMP-2 protein and MMP-9 protein upregulated in comparison to adjacent tissue group （P＜0.05）. The significant association was found between the expre-ssion of E-cadherin and the gastric cancer tissues of T3＋T4 stage， N1-N3 stage， and Ⅲ＋Ⅳ stage， which had lower positive expression rate （P＜0.05）. The expression of MMP-2 protein in gastric cancer tissues of M1 stage and Ⅲ＋Ⅳstage upregulated （P＜0.05）， and the expression of MMP-9 protein upregulated in gastric cancer tissues of T3＋T4 stage，Ⅲ＋Ⅳ stage， or lowlydifferentiated＋undifferentiated （P＜0.05）. No significant relationship was found in other clinical-pathological features and 3 kinds of protein except aforementioned significant relationship （P＞0.05）. Conclusions In the development progress of gastric cancer， the E-cadherin may get involved in the mechanism of tumor invasion and lymph node metastasis， MMP-2 protein may get involved in the mechanism of distant metastasis， and MMP-9 protein may get involved in the mechanism of differentiation and tumor invasion. The examination of those 3 kinds of markers may play an role in the judgment of tumor stage and estimation of prognosis in gastric cancer clinically.
ObjectiveTo investigate the relationship between the expression of vascular endothelial growth factor (VEGF) and matrix metalloproteinase9 (MMP9) and the recurrence or metastasis of hepatocellular carcinoma (HCC).MethodsThe expression of VEGF and MMP9 in 50 HCC tissues and in 30 normal liver tissues were examined by immunochemistry.ResultsThe positive rates of VEGF and MMP9 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 MMP9 and VEGF was very significant (r=0.98，Plt;0.01). The positive rates of VEGF and MMP9 in HCC with metastasis were higher than that of HCC without metastasis.ConclusionVEGF and MMP9 are expressed cooperatively. Both of them play important role in the invasion and metastasis of HCC.
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.
目的 观察局灶性脑缺血梗死区周围层粘连蛋白（Laminin）及基质金属蛋白酶（MMP）-9表达，探讨其在脑缺血再灌注损伤发病机制中的作用。 方法 将45只体重250～300 g、4个月龄的Sprague Dawley（SD）雄性大鼠随机分为假手术（Sham）组与局灶性缺血再灌注（MCAO）组。MCAO组又分6、24、72 h及7 d组，每组各9只。光学显微镜下观察脑组织病理改变，免疫组织化学染色检测各组Laminin及MMP-9的表达情况。 结果 再灌注后6 h，即有MMP-9表达明显增高，表达高峰出现在再灌注后24 h，3 d时有所下降，至7 d时仍明显高于基础水平（P＜0.01）。Laminin的表达于再灌注6 h开始降低，24 h降至最低，3 d后开始缓慢回升。 结论 脑缺血再灌注后，病变区MMP-9与Laminin表达变化可反映脑血管壁受损状况，并与脑缺血损伤及修复过程有关。
目的 探讨不同剂量和不同疗程米非司酮对大鼠子宫异位内膜基质金属蛋白酶-9（MMP-9）及其组织特异性抑制物-1（TIMP-1）表达的影响。 方法 65只子宫内膜异位症大鼠随机分为低剂量组、高剂量组、对照组。各个剂量组分别灌胃20、30、40 d后取异位子宫内膜组织用免疫组织化学法检测MMP-9及TIMP-1的表达，并计算MMP-9/TIMP-1比值。 结果 低剂量组和高剂量组均能使异位内膜MMP-9表达下降（P＜0.05）,TIMP-1表达升高（P＜0.05）,高剂量组的作用更加明显，与低剂量组差异有统计学意义（P＜0.05）；用药30 d低剂量组TIMP-1表达最高，与用药20 d和40 d相比差异有统计学意义（P＜0.05）,同样高剂量组用药30d TIMP-1的表达也最高，与用药20 d和用药40 d比较差异有统计学意义（P＜0.05）。与用药20、40 d比较差异有统计学意义（P＜0.05）。 结论 米非司酮能够降低大鼠异位子宫内膜的侵袭能力，高剂量米非司酮抑制效果更明显；用药30 d米非司酮对大鼠异位内膜的侵袭能力抑制最强，延长用药时间不能使异位内膜侵袭能力继续下降。
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.
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.
【Abstract】ObjectiveTo investigate whether tumor necrosis factor-α (TNF-α) enhance the expression of vascular endothelial growth factor (VEGF) and matrix metalloproteinase-9(MMP-9) in hepatic cancer cell line HepG2 or not. Methods Cultured HepG2 cells were treated by TNF-α with various concentration and time. The morphological changes of HepG2 cells were studied microscopically and the proliferation of HepG2 were detected by methyl thiazolyl tetrazolium (MTT). The expression of VEGF and MMP-9 mRNA in cultured HepG2 were determined by relative quantitative reverse transcription polymerase chain reaction. The VEGF and MMP-9 protein level in supernatants and in cytoplasm were determined by enzymelinked immunosorbent assay (ELISA) and by immunocytochemical staining, respectively.Results There was a little morphological changes in HepG2 with TNF-α treatment, but no change of cell proliferation in corresponding time. The expression of VEGF and MMP-9 mRNA was enhanced gradually with the TNF-α concentration increasing, the VEGF and MMP-9 protein level in supernatants and in cytoplasm was elevated gradually with the concentration increasing. There was a dependance on the concentration when the concentration of TNF-α was lower than or equal to 104 U/L. Furthermore, the effect of promotion was close to peak when the TNF-α concentration up to 104 U/L; but no timeeffect pattern observed. Conclusion TNF-αJP can enhance the expression of VEGF and MMP-9 at the level of mRNA and protein in hepatic cancer cell line.
ObjectiveTo study how CD73 is shed from the retinal pigment epithelium (RPE) surface.MethodsCD73 shedding was induced by treating RPE with lipopolysaccharides (LPS) and TNF-α. After Phospholipase C (PLC) or pan matrix metalloproteinase (MMP) inhibitors were added, surface amount of CD73 was evaluated by flow cytometry (FACS). Then selective inhibitors or their corresponding siRNAs of MMP-2 and MMP-9 were applied to the treatments of RPE; and their effects on induced CD73 shedding were evaluated by FACS. By site directed mutagenesis, mutations were introduced to Lys547-Phe548 coding sites of CD73 cDNA, which was cloned in a pcDNA mammalian expression vector. Both wt-CD73 and mutated-CD73 were over expressed in CD73-/- RPE and their induced shedding was compared.ResultsLPS and TNF-α induced CD73 shedding from RPE was completely blocked by the addition of pan MMP inhibitor but not PLC inhibitor. Selective MPP-9, but not MMP-2, inhibitor or its siRNA blocked CD73 shedding. In CD73-/- RPE induced CD73 shedding was happened to overexpressed wt-CD73 but not Lys547-Phe548 sites mutant CD73.ConclusionMMP-9 is responsible for shedding CD73 from RPE through hydrolyzing its Lys547 -Phe548 sites.