Hospital of Taishan Medical College
Hospital of Taishan Medical College
Wu J.,Shandong University |
Liu F.,Shandong University |
Zhao J.,Shandong University |
Wei Y.,Shandong University |
And 8 more authors.
Cell Biochemistry and Function | Year: 2013
This study aimed to identify the role and regulation of thymic stromal lymphopoietin (TSLP) in asthmatic airway remodelling. To identify the expression of TSLP, α smooth muscle actin (α-SMA) and collagen I in bronchial tissues, bronchial biopsy specimens were collected from patients with asthma and healthy controls and stained with specific antibodies, respectively. To characterize the signalling pathways regulated by TSLP, we silenced or overexpressed TSLP in human lung fibroblast (HLF-1) cells by shRNA approaches or transfection and detected the expression of TSLP receptor (TSLPR) by enzyme-linked immunosorbent assay and Western blot analysis. In TSLP signalling pathway, the protein expression of total signal transducer and activator of transcription 3 (STAT3), STAT5, the phosphorylation of STAT3 (pSTAT3) and STAT5 (pSTAT5), TSLP, α-SMA and collagen I were also detected by Western blotting. In addition, the α-SMA, collagen I and mRNA expression were determined by real-time reverse-transcription. To further confirm the TSLP-STAT3 signalling pathway in HLF-1 cells, we inhibited STAT3 activity by targeted small molecules and then detected TSLP-induced expression of α-SMA and collagen I in both mRNA and protein levels by quantitative real-time reverse-transcription and Western blotting, respectively. First, overexpression of TSLP, α-SMA and collagen I was detected in epithelium collected from patients with asthma. Second, STAT3 activity and the expression of α-SMA and collagen I were controlled, regulated by TSLP. Specifically, the pSTAT3, α-SMA and collagen I were induced by the introduction of TSLP in HLF-1 cells, and the repression of α-SMA and collagen I was detected after TSLP silencing. Third, no changes of pSTAT5 were found in the presence of the STAT3 inhibitor, and TSLP-induced α-SMA and collagen I upregulation is in a STAT3 dependent manner. If we inhibit STAT3 activity by STAT3 targeted small molecules, TSLP-induced α-SMA and collagen I upregulation cannot be detected. The functions of TSLP in asthmatic airway remodelling were performed through STAT3 signalling pathway. © 2012 John Wiley & Sons, Ltd.
Zhang Y.-B.,Hospital of Taishan Medical College |
Yang M.-F.,Hospital of Taishan Medical College |
Sun B.-L.,Hospital of Taishan Medical College |
Niu J.-Z.,Hospital of Taishan Medical College
Journal of Clinical Rehabilitative Tissue Engineering Research | Year: 2010
Background: Ischemic, hypoxic, hypoxia and other stimuli can lead to endogenous neural stem cell proliferation and differentiation, which play a role in brain repair, but it is still not clear whether hypoxic preconditioning can affect the proliferation of endogenous neural stem cells. Objective: To explore the proliferation of endogenous neural stem cells in hippocampus of hypoxic preconditioning mice. Methods: Balb/c clean mice were randomly divided into three groups. Mice in the hypoxia control group were placed in a wide-mouthed bottle, blocked by rubber stopper. Animals with the first asthmoid respiration marked tolerance limit of hypoxia, and once hypoxia exposure was completed. Above-mentioned procedures were repeated four times in the hypoxic preconditioning group. Mice in the normal control group were not exposed to hypoxia. The number and fluorescence intensity of BrdU-labeled cells were counted and observed by immunofluorescence and confocal laser scanning microscope. Results And Conclusion: Compared with hypoxia control group, the tolerance time was significantly longer in the hypoxic preconditioning group (P < 0.01). Fluorescence intensity of BrdU-labeled endogenous neural stem cells was faint, and a few BrdU-positive cells were visible in the hippocampus in the normal control group. The fluorescence intensity and BrdU-positive cell number were significantly increased in the hypoxia control and hypoxic preconditioning groups (P < 0.01). The increased range was greater in the hypoxic preconditioning group compared with the hypoxia control group (P < 0.01). Results suggest that proliferation of endogenous neural stem cells is seen obviously in hippocampus of hypoxic preconditioning mice, which is perhaps involved in cerebral protective mechanism of hypoxic preconditioning.