IMS To isolate mouse CCR5 cDNA (muCCR5) and study its expression in vivo.METHODS Marathon PCR was used to isolate muCCR5 cDNA and two animal models were designed to investigate the gene expression in vivo, one was m...IMS To isolate mouse CCR5 cDNA (muCCR5) and study its expression in vivo.METHODS Marathon PCR was used to isolate muCCR5 cDNA and two animal models were designed to investigate the gene expression in vivo, one was mouse fulminant hepatitis induced by Propionibacterium acnes (P.acnes) and the other was that with delayed type hypersensitivity reaction (DTH). A specific GSTNH2terminus of muCCR5 fusion protein antibody F(ab′)2 was prepared and clarified. RTPCR and immunohistochemical analysis were used to observe the expression level of CCR5 gene in mice.RESULTS A positive reaction of mouse macrophage was found in DTH but not expressed in P.acnes induced fulminant hepatitis by RTPCR and immunohistochemical analysis.CONCLUSION This muCCR5 expression may be involved in an allergic process mediated by cellular immunity but not acute inflammatory reaction induced by P.acnes..展开更多
Background Endoplasmic reticulum （ER） stress and ER stress-mediated apoptosis were reported to be involved in the pathogenesis of several diseases. In a recent study, it was reported that the ER stress pathway was a...Background Endoplasmic reticulum （ER） stress and ER stress-mediated apoptosis were reported to be involved in the pathogenesis of several diseases. In a recent study, it was reported that the ER stress pathway was activated in the lungs of lipopolysaccharide （LPS）-treated mice. It was also found that the C/EBP homologous protein （CHOP）, an apoptosis-related molecule, played a key role in LPS-induced lung damage. The aim of this study was to verify whether LPS could activate the ER stress response in airway epithelial cells and which molecule was involved in the pathway. This study was also aimed at finding new reagents to protect the airway epithelial cells during LPS injury. Methods ER stress markers were observed in LPS-incubated NCI-H292 cells. SiRNA-MUC5AC was transfected into NCI-H292 cells. The effects of dexamethasone and erythromycin were observed in LPS-induced NCI-H292 cells. Results LPS incubation increased the expression of ER stress markers at the protein and mRNA levels. The knockout of MUC5AC in cells attenuated the increase in ER stress markers after incubation with LPS. Dexamethasone and erythromycin decreased caspase-3 activity in LPS-induced NCI-H292 cells. Conclusions LPS may activate ER stress through the overexpression of MUC5AC. Dexamethasone may protect human airway epithelial cells against ER stress-related apoptosis by attenuating the overload of MUC5AC.展开更多
文摘IMS To isolate mouse CCR5 cDNA (muCCR5) and study its expression in vivo.METHODS Marathon PCR was used to isolate muCCR5 cDNA and two animal models were designed to investigate the gene expression in vivo, one was mouse fulminant hepatitis induced by Propionibacterium acnes (P.acnes) and the other was that with delayed type hypersensitivity reaction (DTH). A specific GSTNH2terminus of muCCR5 fusion protein antibody F(ab′)2 was prepared and clarified. RTPCR and immunohistochemical analysis were used to observe the expression level of CCR5 gene in mice.RESULTS A positive reaction of mouse macrophage was found in DTH but not expressed in P.acnes induced fulminant hepatitis by RTPCR and immunohistochemical analysis.CONCLUSION This muCCR5 expression may be involved in an allergic process mediated by cellular immunity but not acute inflammatory reaction induced by P.acnes..
文摘Background Endoplasmic reticulum （ER） stress and ER stress-mediated apoptosis were reported to be involved in the pathogenesis of several diseases. In a recent study, it was reported that the ER stress pathway was activated in the lungs of lipopolysaccharide （LPS）-treated mice. It was also found that the C/EBP homologous protein （CHOP）, an apoptosis-related molecule, played a key role in LPS-induced lung damage. The aim of this study was to verify whether LPS could activate the ER stress response in airway epithelial cells and which molecule was involved in the pathway. This study was also aimed at finding new reagents to protect the airway epithelial cells during LPS injury. Methods ER stress markers were observed in LPS-incubated NCI-H292 cells. SiRNA-MUC5AC was transfected into NCI-H292 cells. The effects of dexamethasone and erythromycin were observed in LPS-induced NCI-H292 cells. Results LPS incubation increased the expression of ER stress markers at the protein and mRNA levels. The knockout of MUC5AC in cells attenuated the increase in ER stress markers after incubation with LPS. Dexamethasone and erythromycin decreased caspase-3 activity in LPS-induced NCI-H292 cells. Conclusions LPS may activate ER stress through the overexpression of MUC5AC. Dexamethasone may protect human airway epithelial cells against ER stress-related apoptosis by attenuating the overload of MUC5AC.
