To investigate whether apoptosis is associated with cell adhesion in bronchial epithelium, and whether it contributes to the kinetics of injury and repair of surface epithelia, this study was performed for E-cadherin expression by using immunohistochemistry technique and for apoptosis by TUNEL method. An animal model of smoking was used for this study. The results showed that epithelial cells with membrane anchored E-cadherin decreased remarkably at several time points during 6 months of exposure to smoke (P < 0.01) and then restored to normal level. This fluctuation was associated exclusively with the alteration in number of apoptotic cells (P < 0.01). There was no significant difference in activation of nuclear transcription factor NF-kappa B among groups (P > 0.05). All these suggested that apoptosis is associated with E-cadherin expression in bronchial epithelium of smoking mouse.
*Apoptosis ; Bronchi/metabolism ; Bronchi/*pathology ; Cadherins/analysis ; Cadherins/*biosynthesis ; Epithelial Cells/chemistry ; Epithelial Cells/metabolism ; Epithelial Cells/pathology ; Smoking/*adverse effects

OBJECTIVE: To explore the expression of CCN5 in endometriotic tissues and its impact on proliferation, migration and invasion of human endometrial stromal cells (HESCs). METHODS: We collected ovarian endometriosis samples from 20 women receiving laparoscopic surgery and eutopic endometrium samples from 15 women undergoing IVF-ET for comparison of CCN5 expression. Cultured HESCs were transfected with a recombinant adenovirus Ad-CCN5 for CCN5 overexpression or with a CCN5-specific siRNA for knocking down CCN5 expression, and the changes of cell proliferation, migration and invasion were evaluated using CCK-8 assay, wound healing assay and Transwell chamber assay. RT-qPCR and Western blotting were used to examine the expression levels of epithelial-mesenchymal transition (EMT) markers including E-cadherin, N-cadherin, Snail-1 and vimentin in HESCs with CCN5 overexpression or knockdown. RESULTS: CCN5 expression was significantly decreased in ovarian endometriosis tissues as compared with eutopic endometrium samples (P < 0.01). CCN5 overexpression obviously inhibited the proliferation, migration and invasion of HESCs, significantly increased the expression of E-cadherin and decreased the expressions of N-cadherin, Snail-1 and vimentin (P < 0.01). CCN5 knockdown significantly enhanced the proliferation, migration and invasion of HESCs and produced opposite effects on the expressions of E-cadherin, N-cadherin, Snail-1 and vimentin (P < 0.01). CONCLUSION CCN5 can regulate the proliferation, migration and invasion of HESCs and thus plays an important role in EMT of HESCs, suggesting the potential of CCN5 as a therapeutic target for endometriosis.
Cell Movement ; Cell Proliferation ; Endometriosis/metabolism* ; Endometrium/metabolism* ; Epithelial Cells ; Epithelial-Mesenchymal Transition ; Female ; Humans ; Stromal Cells

The purpose of this study was to establish a three-dimensional (3D) organoid culture system for type 2 alveolar epithelial (AT2) cells in mice. AT2 cells were isolated from ICR mouse lung and purified by enzymatic digestion and MicroBeads sorting. The purity of AT2 cells was determined by immunofluorescence (IF) staining using an antibody against proSPC. The AT2 differentiation was examined by IF staining with proSPC/HopX and proSPC/T1α antibodies, and proliferation of AT2 cells was assessed by EdU incorporation assays after two-dimensional (2D) culture for 8 days. In addition, AT2 cells were co-cultured with mouse lung fibroblasts (Mlg) in three-dimensional (3D) culture system. After 13 days of co-culture, the organoids were fixed in 2% paraformaldehyde for histological analysis and IF staining. The results showed that the purity of the AT2 cells was over 95%, as assessed by proSPC staining. 2D cultured AT2 cells were negative for EdU staining, which indicates that no proliferation occurs. proSPC expression was gradually disappeared, whereas T1α and HopX expression was gradually increased after 3, 5 and 8 days of culture. In 3D culture system, the alveolar organoids were formed after co-culturing AT2 cells with Mlg for 4 days. Histological analysis showed that alveolar organoids displayed a hollow morphology. proSPC was highly expressed in the peripheral cells, whereas type 1 alveolar epithelial (AT1) cells transdifferentiated from AT2 cells expressing HopX were mainly located in the interior of organoid bodies after 13 days. Some of the proSPC-positive AT2 cells located in the outer circle of alveolar organoids were stained positive for both proSPC and EdU, indicating that the AT2 cells in the alveolar organoids were proliferative. These results showed that the 3D organoid culture system of mouse AT2 cells was successfully established.
Alveolar Epithelial Cells/metabolism* ; Animals ; Cell Differentiation ; Cells, Cultured ; Epithelial Cells ; Lung ; Mice ; Mice, Inbred ICR ; Organoids

Phosphorylation of beta-catenin tyrosine residue 654 plays an important role in the epithelial to myofibroblast transition (EMT). Introducing mimic peptide of tyrosine residue 654 domain of beta-catenin into cells may influence phosphorylation of beta-catenin tyrosine residue 654. To deliver this mimic peptide into renal epithelial cells, we used penetratin as a vector, which is a novel cell permeable peptide, to deliver hydrophilic molecules into cells. A tyrosine 654 residue domain mimic peptide of beta-catenin (PM) with fused penetratin was constructed, purified and then detected for the penetration of the mimic peptide into human renal tubular epithelial cells (HK-2). The results showed that purified fusion mimic peptide could efficiently and rapidly translocate into human renal tubular epithelial cells. It is concluded that a cell-permeable peptides mimic of tyrosine residue 654 domain of beta-catenin was successfully obtained, which may provide a useful reagent for interfering the human renal tubular epithelial-mesenchymal transition.
Carrier Proteins/*metabolism ; Epithelial Cells/cytology ; Epithelial Cells/*metabolism ; Fibroblasts/cytology ; Fibroblasts/metabolism ; Kidney Tubules/*cytology ; Peptides/metabolism ; Permeability ; Phosphorylation ; Tyrosine/*metabolism ; beta Catenin/*metabolism

Animals ; Calpain ; metabolism ; Epithelial Cells ; metabolism ; Kidney ; cytology ; Kidney Tubules ; cytology ; metabolism ; Rats ; Reperfusion Injury ; metabolism

Animals ; Humans ; Thymic Stromal Lymphopoietin ; Pyroglyphidae/metabolism* ; Cytokines/metabolism* ; Asthma/metabolism* ; Respiratory System ; Epithelial Cells/metabolism*

Objective: Fine particulate matter (PM _2.5) is an air pollutant that has become of great concern in recent years. Numerous studies have found that PM _2.5 may contribute to lung cancer, but the pathogenesis has not yet been fully elucidated. In this study, we explored the roles of exosomes from bronchial epithelial cells in PM _2.5-promoted lung cancer metastasis. Methods: Exosomes were isolated from cell supernatants. An animal model of lung metastasis (established by tail vein injection of A549-luc) and in vitro studies with lung cancer cell lines were used to investigate the effects of exosomes derived from PM _2.5-treated human bronchial epithelial cells (PHBE-exo). Results: The animal experiments revealed that PHBE-exo-treated mice showed stronger luciferase activity and a larger relative metastatic region in the lungs, thus indicating that PHBE-exo promoted the metastatic potential of lung cancer. Additionally, PHBE-exo promoted the migration, invasion and epithelial-to-mesenchymal transition of lung cancer cells, in a manner mediated by activation of c-Jun N-terminal kinase. Conclusion These results implied that PM _2.5 may promote the development of lung cancer through exosomes derived from bronchial epithelial cells, thus providing a potential interventional target for lung cancer. These findings broadened our understanding of cancer-promoting mechanisms of environmental pollutants.
Animals ; Epithelial Cells/metabolism* ; Epithelial-Mesenchymal Transition ; Exosomes/metabolism* ; Humans ; Lung Neoplasms/metabolism* ; Mice ; Particulate Matter/toxicity*

OBJECTIVE: To detect cyclooxygenase-2 (COX-2) expression and prostaglandin E2 (PGE2) release in human nasal epithelia (HNE) induced by lipopolysaccharide (LPS) in different concentration gradient and time gradient, and to investigate their roles in nasal inflammatory pathogenesis. METHOD: Western Blot and fluorescent real time quantitative PCR were performed to detect the expression of COX-2 in HNE induced by LPS and blocked by selective inhibitor of COX-2. The concentrations of PGE2 were determined by enzyme immunoassay. RESULT: Low expressions of COX-2 and PGE2 were detected in normal HNE. COX-2 expression and PGE2 release increased in HNE induced by LPS in time-dependent or dose-dependent manner. The increased release of PGE2 was later than that of COX-2 expression. COX-2 expression and PGE2 release were dose-dependently attenuated by selective inhibitor of COX-2. CONCLUSION LPS effectively induces COX-2 expression and PGE2 release in HNE. And COX-2 is responsible for the synthesis of PGE2. These results indicate that the increased expression of COX-2 and PGE2 is involved in the inflammation of HNE induced by LPS in vitro.
Cells, Cultured ; metabolism ; Cyclooxygenase 2 ; metabolism ; Dinoprostone ; biosynthesis ; metabolism ; Epithelial Cells ; metabolism ; Humans ; Lipopolysaccharides ; Nasal Mucosa ; cytology ; metabolism

Somatostatin (SST) is an inhibitory polypeptide hormone that plays an important role in a variety of biological processes. Somatostatin receptor 2 (SSTR2) is the most widely expressed somatostatin receptor. However, the specific cell types expressing Sstr2 in the tissues have not been investigated. In this study, we detected the expression pattern of SSTR2 protein in mouse at different development stages, including the embryonic 15.5 days and the postnatal 1, 7, 15 days as well as 3 and 6 months, by multicolour immunofluorescence analyses. We found that Sstr2 was expressed in some specific cells types of several tissues, including the neuronal cells and astrocytes in the brain, the mesenchymal cells, the hematopoietic cells, the early hematopoietic stem cells, and the B cells in the bone marrow, the macrophages, the type Ⅱ alveolar epithelial cells, and the airway ciliated cells in the lung, the epithelial cells and the neuronal cells in the intestine, the hair follicle cells, the gastric epithelial cells, the hematopoietic stem cells and the nerve fibre in the spleen, and the tubular epithelial cells in the kidney. This study identified the specific cell types expressing Sstr2 in mouse at different developmental stages, providing new insights into the physiological function of SST and SSTR2 in several cell types.
Mice ; Animals ; Receptors, Somatostatin/metabolism* ; Hematopoietic Stem Cells/metabolism* ; Epithelial Cells

No abstract available.
Animal ; Chloride Channels/metabolism ; Chloride Channels/biosynthesis* ; Choroid Plexus/metabolism* ; Choroid Plexus/cytology ; Epithelial Cells/metabolism*