Objective To investigate the molecular mechanism of nectin-like molecule 1(NECL1) inhibiting the migration and invasion of U251 glioma cells.Methods We infected U251 glioma cells with adeno-nectin-like molecule 1(Ad-N...Objective To investigate the molecular mechanism of nectin-like molecule 1(NECL1) inhibiting the migration and invasion of U251 glioma cells.Methods We infected U251 glioma cells with adeno-nectin-like molecule 1(Ad-NECL1) or empty adenovirus(Ad).Transwell and wound healing assays were performed to observe the migration of U251 cells incubated with the cell supernatant from Ad-NECL1 or Ad infected U251 cells.DNA microarray was applied to screen the gene expression profile after the restoration of NECL1 in U251 glioma cell lines.The differential expression of osteopontin(OPN),a gene related to migration and invasion,was further analyzed with semi-quantitative reverse transcription-polymerase chain reaction(RT-PCR),Western blot,and immunohistochemistry.Results The restoration of NECL1 inhibited migration of U251 cells significantly(P<0.05).Altogether 195 genes were found differentially expressed by microarray,in which 175 were up-regulated and 20 down-regulated,including 9 extracellular matrix proteins involved in the migration of cells.Both mRNA and protein expressions of OPN,the most markedly reduced extracellular matrix protein,were found decreased in U251 cells after restoration of NECL1.Immunohistochemical assay also detected an increase of OPN in glioma tissues,related with the progressing of malignant grade.Conclusion A link might exist between NECL1 and the extracellular matrix protein OPN in inhibiting the migration and invasion of U251 glioma cells.展开更多
Objectives To evaluate the expression profile of myoD microRNA-29 （miR-29） family in L6 myoblast differentiated to myotube or L6 myotube treated by glucose and insulin, and to further probe the molecular mechanism o...Objectives To evaluate the expression profile of myoD microRNA-29 （miR-29） family in L6 myoblast differentiated to myotube or L6 myotube treated by glucose and insulin, and to further probe the molecular mechanism of myoD regulating the expression of miR-29 clusters.展开更多
Objective The aim of the study was to determine whether bronchial asthma was associated with increased levels of soluble intercellular adhesion molecule 1(sICAM 1) in serum, which might be ...Objective The aim of the study was to determine whether bronchial asthma was associated with increased levels of soluble intercellular adhesion molecule 1(sICAM 1) in serum, which might be valuble data for the effective therapy of these patients Patients and methods The concentrations of sICAM 1 were determined in sera of healthy donors and asthmatic patients using a sensitive enzyme immunoassay Results The mean(±SD) levels of serum sICAM 1 of 26 asthmatic patients (205±72 0 μg/L)was significantly higher than that of the 30 healthy volunteers (154±63 9 μg/L,P<0 01) There was no much difference between the serum levels in 12 patients suffering from atopic asthma and the levels in 14 patients with nonatopic asthma The serum concentrations of sICAM 1 were higher during asthma attacks than that during remissions in the same patients (P<0 05) Conclusion These results suggest that sICAM 1 may play a certain role in the pathophysiology of bronchial asthma,and might be signals for successful treatment展开更多
Objective: To demonstrate the functional changes of gap junctional mediation of intercellular communication in detrusor instability (DI) and its mechanisms. Methods: The function of gap junctional intercellular commun...Objective: To demonstrate the functional changes of gap junctional mediation of intercellular communication in detrusor instability (DI) and its mechanisms. Methods: The function of gap junctional intercellular communication in the cultured bladder detrusor cells was detected by fluorescence redistribution after photobleaching. Results: At the fourth minute after bleaching, the mean fluorescences recovery rates of DI group bladder detrusor cells were (35 791±0 836)%, that of control group (8 645±0 673)%. The mean fluorescence recovery rates of DI group were significantly higher than those of control group ( P <0 01). Conclusion: It shows that the increase of intercellular excitatory communication is one of the important reasons of pathogenesis of DI.展开更多
Objective： To investigate the effect of oridonin on proliferation and invasion of human multiple myeloma LP-1 ceils and the underlying mechanism. Methods： LP-1 cells in culture medium in vitro were treated with orid...Objective： To investigate the effect of oridonin on proliferation and invasion of human multiple myeloma LP-1 ceils and the underlying mechanism. Methods： LP-1 cells in culture medium in vitro were treated with oridonin at the different concentration Cell proliferation was measured by Microwave Theory and Techniques （MTT） assay and cell apoptotic rate was detected by flow cytometry. Morphology of cell apoptosis was observed by transmission electron microscope. Expressions of Bax, Bcl-2, Caspase-3, NFqcB as well as I-~B mRNA were detected by real-time PCR. Results： The MTT assays and flow cytometry revealed that oridonin could inhibit the growth of LP-1 cells and cause apoptosis significantly; the suppression was both in time- and dose-dependent manner. Marked morphological changes of cell apoptosis were found under a transmission electron microscope after the cells were treated with oridonin at 25 ~rnol/L for 24 h. Along with the apoptotic process, Bcl-2, Caspase-3,NF-r,.B gene expressions were down-regulated （P〈0.05）. On the contrast, the Bax and I-~zB gene expressions were up-regulated （P〈0.05）. Conclusion： Oridonin could inhibit the proliferation of LP-1 cells via inducing apoptosis. We concluded that oridonin induces apoptosis in LP-1 cells via activation of caspase-3 as well as down-regulation of Bcl-2 and up-regulation of Bax expression. The results suggested that oridonin could induce apoptosis of LP-1 cells through mitochondria- and caspase3-dependent pathways. Meanwhile, the inhibition of NF-r,_B and the activation of I-~B indicate pro-apoptotic stimuli. In one word, oridonin might be an important potential anti-myeloma reagent.展开更多
基金Supported by National Natural Science Foundation of China (30421003,30828004)
文摘Objective To investigate the molecular mechanism of nectin-like molecule 1(NECL1) inhibiting the migration and invasion of U251 glioma cells.Methods We infected U251 glioma cells with adeno-nectin-like molecule 1(Ad-NECL1) or empty adenovirus(Ad).Transwell and wound healing assays were performed to observe the migration of U251 cells incubated with the cell supernatant from Ad-NECL1 or Ad infected U251 cells.DNA microarray was applied to screen the gene expression profile after the restoration of NECL1 in U251 glioma cell lines.The differential expression of osteopontin(OPN),a gene related to migration and invasion,was further analyzed with semi-quantitative reverse transcription-polymerase chain reaction(RT-PCR),Western blot,and immunohistochemistry.Results The restoration of NECL1 inhibited migration of U251 cells significantly(P<0.05).Altogether 195 genes were found differentially expressed by microarray,in which 175 were up-regulated and 20 down-regulated,including 9 extracellular matrix proteins involved in the migration of cells.Both mRNA and protein expressions of OPN,the most markedly reduced extracellular matrix protein,were found decreased in U251 cells after restoration of NECL1.Immunohistochemical assay also detected an increase of OPN in glioma tissues,related with the progressing of malignant grade.Conclusion A link might exist between NECL1 and the extracellular matrix protein OPN in inhibiting the migration and invasion of U251 glioma cells.
基金Supported by the National Nature Science Foundation of China(81100608 and 30901342)
文摘Objectives To evaluate the expression profile of myoD microRNA-29 （miR-29） family in L6 myoblast differentiated to myotube or L6 myotube treated by glucose and insulin, and to further probe the molecular mechanism of myoD regulating the expression of miR-29 clusters.
文摘Objective The aim of the study was to determine whether bronchial asthma was associated with increased levels of soluble intercellular adhesion molecule 1(sICAM 1) in serum, which might be valuble data for the effective therapy of these patients Patients and methods The concentrations of sICAM 1 were determined in sera of healthy donors and asthmatic patients using a sensitive enzyme immunoassay Results The mean(±SD) levels of serum sICAM 1 of 26 asthmatic patients (205±72 0 μg/L)was significantly higher than that of the 30 healthy volunteers (154±63 9 μg/L,P<0 01) There was no much difference between the serum levels in 12 patients suffering from atopic asthma and the levels in 14 patients with nonatopic asthma The serum concentrations of sICAM 1 were higher during asthma attacks than that during remissions in the same patients (P<0 05) Conclusion These results suggest that sICAM 1 may play a certain role in the pathophysiology of bronchial asthma,and might be signals for successful treatment
文摘Objective: To demonstrate the functional changes of gap junctional mediation of intercellular communication in detrusor instability (DI) and its mechanisms. Methods: The function of gap junctional intercellular communication in the cultured bladder detrusor cells was detected by fluorescence redistribution after photobleaching. Results: At the fourth minute after bleaching, the mean fluorescences recovery rates of DI group bladder detrusor cells were (35 791±0 836)%, that of control group (8 645±0 673)%. The mean fluorescence recovery rates of DI group were significantly higher than those of control group ( P <0 01). Conclusion: It shows that the increase of intercellular excitatory communication is one of the important reasons of pathogenesis of DI.
文摘Objective： To investigate the effect of oridonin on proliferation and invasion of human multiple myeloma LP-1 ceils and the underlying mechanism. Methods： LP-1 cells in culture medium in vitro were treated with oridonin at the different concentration Cell proliferation was measured by Microwave Theory and Techniques （MTT） assay and cell apoptotic rate was detected by flow cytometry. Morphology of cell apoptosis was observed by transmission electron microscope. Expressions of Bax, Bcl-2, Caspase-3, NFqcB as well as I-~B mRNA were detected by real-time PCR. Results： The MTT assays and flow cytometry revealed that oridonin could inhibit the growth of LP-1 cells and cause apoptosis significantly; the suppression was both in time- and dose-dependent manner. Marked morphological changes of cell apoptosis were found under a transmission electron microscope after the cells were treated with oridonin at 25 ~rnol/L for 24 h. Along with the apoptotic process, Bcl-2, Caspase-3,NF-r,.B gene expressions were down-regulated （P〈0.05）. On the contrast, the Bax and I-~zB gene expressions were up-regulated （P〈0.05）. Conclusion： Oridonin could inhibit the proliferation of LP-1 cells via inducing apoptosis. We concluded that oridonin induces apoptosis in LP-1 cells via activation of caspase-3 as well as down-regulation of Bcl-2 and up-regulation of Bax expression. The results suggested that oridonin could induce apoptosis of LP-1 cells through mitochondria- and caspase3-dependent pathways. Meanwhile, the inhibition of NF-r,_B and the activation of I-~B indicate pro-apoptotic stimuli. In one word, oridonin might be an important potential anti-myeloma reagent.
