Objective To detect the expressions of osteopontin （OPN）， breast tumor kinase （Brk）， and vascular endothelial growth factor （VEGF） in the breast cancer tissue， the adjacent （2cm） normal breast tissue， and the distal（＞5cm） normal breast tissue， and analyze their clinical significances. Method The immunohistochemical method was used to detect the expressions of OPN， Brk， and VEGF in the breast cancer tissue， the adjacent （2cm） normal breast tissue， and the distal （＞5cm） normal breast tissue from 40 cases of breast cancer. Results ① The expressions of OPN，Brk， and VEGF in the breast cancer tissue were significantly higher than those of the adjacent （2cm） normal breast tissue and the distal （＞5cm） normal breast tissue （P＜0.01）， the expression of Brk in the adjacent （2cm） normal breast tissue was significantly higher than that of the distal （＞5 cm） normal breast tissue （P＜0.05）. ② In the breast cancer tissue， the OPN and Brk protein expressions were not associated with age， tumor diameter， and histological grade （P＞0.05），were associated with lymph node metastasis and TNM stage （P＜0.05）. The VEGF protein expression was not associated with age and tumor diameter （P＞0.05）， but was associated with histological grade， lymph node metastasis， and TNM staging （P＜0.05）. ③ In the breast cancer tissue， OPN， Brk， and VEGF had positive correlation with each other （P＜0.05）， but not in the adjacent （2cm） normal breast tissue and the distal （＞5 cm） normal breast tissue （P＞0.05）. Conclusions The expressions of OPN and Brk from the same signal pathway increase by turns in the distal （＞5 cm） normal breast tissue， adjacent （2cm） normal breast tissue， and breast cancer tissue. OPN induced the adhesion and migration of endothelial cells to accelerate vascular repair through VEGF and Brk has correlation with the progress of tumor invasion and metastasis through participating in tumor vascularization.
ObjectiveTo explore the role of osteopontin (OPN) in hyperoxia-induced acute lung injury and its relationship with nuclear factor-κB (NF-κB),matrix metalloproteinase 2 and 9 (MMP-2,MMP-9). MethodsNinety-six mice were randomly divided into a phosphate buffer solution intranasal inhalation group (PBS group) and a recombinant OPN intranasal inhalation group. The mice were exposed in sealed cages >95% oxygen for 24-72 hours to induce lung injury or room air as control. The severity of lung injury was evaluated. The expression of NF-κB,MMP-2,MMP-9,TIMP-1 and TIMP-2 mRNA in lung tissue at 24,48 and 72 hours under hyperoxia were examined by reverse transcript-polymerase chain reaction (RT-PCR). Immunohistochemistry (IHC) was performed for detection of NF-κB protein in lung tissue. ResultsPBS group mice developed more severe acute lung injury at 72 hours under hyperoxia.TIMP-1 and TIMP-2 mRNA expressions were significantly increased in r-OPN group than their matched PBS group when exposed to hyperoxia. IHC study showed higher expression of NF-κB protein in lung tissue of PBS group at 72 hours of hyperoxia. ConclusionOPN can protect against hyperoxia-induced lung injury by inhibiting the expressions of NF-κB,MMP-2 and MMP-9.
ObjectiveTo investigate the role of osteopontin (OPN) on the expressions of matrix metalloproteinase 13 (MMP-13) mRNA and protein in human knee osteoarthritic chondrocytes and to find the optimal time and concentration for OPN treatment. MethodsChondrocytes were isolated from articular cartilage tissues of patients with primary osteoarthritis (OA) and cultured using one step digestive treatment with collagenase typeⅡ. The chondrocytes were then identified using immunohistochemistry of collagen typeⅡ. The first generation of chondrocytes were stimulated with OPN at a concentration of 1μg/mL for 0, 24, 48, and 72 hours, and with OPN at the concentrations of 0, 0.5, 1, 2, and 4μg/mL for 48 hours. The levels of MMP-13 mRNA and protein expressions were measured with real-time fluorescent quantitative PCR and Western blot. ResultsThe immunohistochemical staining showed that first generation of chondrocytes expressed collagen typeⅡ. Both MMP-13 mRNA and protein expression levels in OA chondrocytes increased significantly in the presence of OPN (1μg/ mL) and peaked at 48 hours after incubation, showing significant difference between different time points (P < 0.05). The MMP-13 mRNA expression level in OA chondrocytes at the OPN concentration of 1μg/mL was significantly higher than those at the other concentrations (P < 0.05), and the MMP-13 protein expression level at the OPN concentration of 1μg/mL was significantly higher than that at 0μg/mL (P < 0.05). MMP-13 protein expression level at the OPN concentrations of 0.5, 2, and 4μg/mL were significantly higher than that at 0μg/mL (P < 0.05). ConclusionOPN induces up-regulation of MMP-13 mRNA and protein expressions in human knee osteoarthritic chondrocytes in time-and dose-dependent manners. The optimal time and concentration for OPN treatment are 48 hours and 1μg/mL, respectively.
ObjectiveTo systematically review the association between expression of osteopontin (OPN) and Chinese population with hepatocellular carcinoma (HCC) and its clinical pathological characteristics. MethodsSuch databases including CBM, CNKI, VIP and WanFang Data were searched from inception to July 2014, for studies about the association between expression of OPN and Chinese population with HCC and its clinical pathological characteristics. Two reviewers independently screened literature according to the exclusion and inclusion criteria, extracted data, and assessed methodological quality of included studies. Then, meta-analysis was performed using RevMan 5.2 software. ResultsA total of 10 case-control studies (involving 723 HCC cases and 102 controls) were included. The results of meta-analysis showed that:OPN expression was higher in HCC group than normal control group (OR=10.25, 95%CI 6.13 to17.14); and higher in imperfect capsular infiltration group than perfect capsular infiltration group (OR=2.71, 95%CI 1.58 to 4.64). However, no significant difference was found in OPN expression between isolated tumour group and multiple tumours group (OR=0.95, 95%CI 0.56 to 1.62); between high differentiation group and low differentiation group (OR=0.60, 95%CI 0.36 to 1.01); and between clinical stages I-Ⅱ group and clinical stages Ⅲ-IV group (OR=0.93, 95%CI 0.53 to 1.63). ConclusionCurrent evidence shows that OPN may take part in the whole course (occurrence and advance) of HCC in Chinese population, but the problem whether it can be used as a factor to evaluate prognosis needs to be further studied.
ObjectiveTo investigate the effect of azithromycin on chronic obstructive pulmonary disease (COPD) vascular remodeling and its possible mechanism.MethodsEighteen male SD rats were randomly divided into normal control group (group A), model group (group B) and azithromycin intervention group (group C). In group B and group C, the COPD model was established by passive smoking and intratracheal injection of lipopolysaccharide. On the fifteenth day, group C was intragastricly administrated with azithromycin (50 mg/kg) one hour prior to smoking, while group A and group B were given equal amount of normal saline. All the rats were killed 6 weeks later. Hematoxylin-eosin staining was used to observe lung tissue pathological changes and victoria blue + Van Gieson staining was used to observe the pulmonary artery morphology changes. The serum osteopontin (OPN) was determined with ELISA. The protein expression of OPN was measured with immunohistochemistry and OPN mRNA was detected by RT-PCR.ResultsCompared with group A, the degree of pulmonary vascular inflammation and pulmonary vascular remodeling in groups B and C was more serious, but these changes in group C were lighter than those in group B. The serum OPN content, lung tissue OPN protein and OPN mRNA expression in groups B and C were higher than those in group A, while these parameters in group C were lower than those in group B. The content of serum OPN, the expression of OPN protein and OPN mRNA in lung tissue were positively correlated with the degree of pulmonary vascular inflammation and vascular remodeling.ConclusionAzithromycin can alleviate the pulmonary vascular inflammation and pulmonary vascular remodeling in COPD rats, and its mechanism may be related to inhibiting the expression of OPN.