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

This study was purposed to investigate the relationship between the catalysis of Bence Jones protein (BJP) in urine of patients with multiple myeloma(MM) and toxicity on the renal proximal tubular cells in vitro, and to explore the potential mechanism for the toxicity of BJP to renal impairment in patients with MM. The Michaelis-Menten constant (K(m)) and catalytic constant (k(cat)) of the amidase activity of BJP was calculated by Hanes equation. The LLC-PK1 cells were cultured with different concentration of BJP for 24 h, then proliferation of the cells were determined by MTT method and apoptosis were determined by flow cytometry. The results showed that the BJP from the MM patients with renal impairment significantly inhibited cell proliferation, as compared with that from MM patients without renal impairment. The BJP with higher k(cat) had higher toxicity to LLC-PK1 cells. BJP could induce apoptosis and necrosis of LLC-PK1 cells when reached a certain concentration and this effect enhanced with increase of BJP concentration. It is concluded that the catalysis of BJP and its toxicity to renal tubular epithelial cells has a positive correlation, and toxic effect of BJP on renal tubular epithelial cells results from inhibiting proliferation and inducing apoptosis and necrosis of the cells, which may be one of renal impairment mechanisms in MM patients.
Animals ; Bence Jones Protein ; metabolism ; toxicity ; Catalysis ; Coculture Techniques ; Epithelial Cells ; metabolism ; pathology ; Humans ; Kidney ; metabolism ; pathology ; Kidney Tubules ; cytology ; LLC-PK1 Cells ; Multiple Myeloma ; metabolism ; pathology ; Swine

OBJECTIVETo observe the expression of Schwann cell marker GFAP and myoepithelial cell marker alpha-SMA in salivary adenoid cystic carcinoma (ACC), and to evaluate the relationship of GFAP, alpha-SMA and perineural invasion in ACC.

METHODSImmunohistochemical SABC method, double-label immunofluorescence and CLSM were used to detect the expression of GFAP and alpha-SMA proteins in salivary ACC tissue samples.

RESULTSIn salivary ACC tissue samples, both GFAP and alpha-SMA proteins were positive, which were coexpressed in cytoplasm of the same onco-myoepithelial cells.

CONCLUSIONSThere may be Schwann cell differentiation in onco-myoepithelial cell of salivary ACC, and it may be the pathological base of perineural invasion in salivary ACC.

Actins ; metabolism ; Carcinoma, Adenoid Cystic ; metabolism ; pathology ; Epithelial Cells ; metabolism ; pathology ; Glial Fibrillary Acidic Protein ; metabolism ; Humans ; Muscle Cells ; metabolism ; pathology ; Salivary Gland Neoplasms ; metabolism ; pathology ; Schwann Cells ; metabolism ; pathology

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.
Animals ; Apoptosis ; Bronchi ; metabolism ; pathology ; Cadherins ; analysis ; biosynthesis ; Epithelial Cells ; chemistry ; metabolism ; pathology ; Mice ; Smoking ; adverse effects

Animals ; Cell Differentiation ; Cytokines ; metabolism ; Disease Progression ; Epithelial-Mesenchymal Transition ; Extracellular Matrix ; metabolism ; Fibroblasts ; metabolism ; pathology ; Hepatic Stellate Cells ; metabolism ; pathology ; Humans ; Liver ; metabolism ; pathology ; Liver Cirrhosis ; etiology ; metabolism ; pathology ; Stem Cells ; metabolism ; pathology

Alveolar Epithelial Cells ; metabolism ; pathology ; Animals ; Apoptosis ; physiology ; Cell Survival ; physiology ; Cells, Cultured ; Epithelial Cells ; cytology ; physiology ; Genes, bcl-2 ; genetics ; Genes, p53 ; genetics ; Oxidative Stress ; genetics ; Rats

Animals ; Apoptosis ; physiology ; Bile Duct Diseases ; pathology ; Bile Ducts ; cytology ; pathology ; Cell Proliferation ; Epithelial Cells ; metabolism ; pathology ; Humans

Glutamine, the most abundant amino acid in bloodstream, is the preferred fuel source for enterocytes. Glutamine exerts its functions through the activity of its transporters, which are located in cytomembrane, to transport it into or out of intestinal epithelial cells. Intestine is the primary center for glutamine metabolism in the body. As ASCT2 and B(0)AT1 are the most important glutamine transporters in the intestine, it wound be helpful to gain the knowledge of the structure, function, and pathologic changes and control strategy of the two transporters in order to have a better understanding of the metabolism and function of glutamine.
Amino Acid Transport System ASC ; Biological Transport ; Enterocytes ; Epithelial Cells ; metabolism ; pathology ; Glutamine ; metabolism ; Humans ; Intestine, Small ; metabolism

OBJECTIVETo investigate the effects of curcumin (CUR) on pneumocyte apoptosis and CCAAT/enhancer binding protein homologous protein (CHOP) in pulmonary ischemia/reperfusion injury (PIRI) in mice.

METHODSSixty C57BL/6J mice were randomly allocated into six groups (n = 10): Sham operation group (Sham group), ischemia/reperfusion group (I/R group), ischemia/reperfusion + dimethyl sulfoxide group (DMSO group), ischemia/reperfusion + curcumin pre-treated with respectively 100 mg/kg, 150 mg/kg and 200 mg/kg groups (CUR-100 group, CUR-150 group and CUR-200 group). Left lung tissue of each group was excised after reperfusion for 3 h. Wet lung weight to dry lung weight (W/D) and total lung water content (TLW) were tested. The morphological and ultrastructural changes of lung tissue were observed under light microscope and electron microscope, and index of quantitative evaluation for alveolar damage (IQA) was calculated. The expression levels of CHOP and glucose regulated protein 78 (GRP78) were detected by RT-PCR and Western Blot. Apoptosis index (AI) of lung tissue was determined by terminal deoxynucleotidyl transferase mediated dUTP nick end labeling (TUNEL) method.

RESULTSCompared with Sham group, the expression levels of CHOP, GRP78 mRNA and protein were all significantly increased (P < 0.05) in I/R group and DMSO group, W/D, TLW, IQA and AI were all notably higher (P < 0.01); morphological and ultrastructural injury in lung tissue were notably observed in I/R group. Compared with DMSO group, the expression levels of GRP78 mRNA and protein were increased higher (P < 0. 05) in CUR-100 group, CUR-150 group, and CUR-200 group, but the expression levels of CHOP mRNA and protein were decreased lower (P < 0.05), W/D, TLW, IQA and AI were also decreased (P < 0.05, P < 0.01); morphological and ultrastructural injury in lung tissue were gradually alleviated in CUR groups.

CONCLUSIONI/R induces excessive unfolded protein response (UPR) in lung tissue, in which CHOP participates in pneumocyte apoptosis, leading to lung injury; CUR has notable effects on lung protection against I/R injury, which may be related to inhibition of apoptosis mediated by CHOP in excessive UPR.

Alveolar Epithelial Cells ; metabolism ; Animals ; Apoptosis ; Curcumin ; pharmacology ; Heat-Shock Proteins ; metabolism ; Lung ; metabolism ; pathology ; Male ; Mice ; Mice, Inbred C57BL ; Reperfusion Injury ; metabolism ; pathology ; Transcription Factor CHOP ; metabolism

OBJECTIVETo analyze the centrosome abnormalities in the malignant transformation of human bronchial epithelial cells (BEAS-2B) induced by coal tar pitch smoke extracts and to investigate the role and action mechanism of centrosome in the lung cancer induced by coal tar pitch.

METHODSMedium-temperature coal tar pitch smoke extracts were used to treat immortalized human bronchial epithelial cells (BEAS-2B) and establish a malignant transformation model. The treated BEAS-2B cells were used as exposure group, and solvent control group and normal control group were also set for passage culture. The changes of centrosome in BEAS-2B cells seeded on coverslips were evaluated by indirect immunofluorescence assay. The mRNA expression of p53, p21, and cyclin E in BEAS-2B cells was measured by real-time quantitative RT-PCR, and their protein levels in BEAS-2B cells seeded on coverslips were measured by semiquantitative immunohistochemical analysis.

RESULTSThe overall rate of centrosome abnormalities in BEAS-2B cells at passage 20 was 6.56±1.01% in the exposure group, significantly higher than those in the normal control group (3.40±0.86%) and solvent control group (3.14±0.59%) (P < 0.05). In addition, the exposure group had a significantly higher overall rate of centrosome abnormalities in BEAS-2B cells at passage 30 compared with the normal control group and solvent control group (22.39±9.5% vs 4.34±1.04%, P < 0.05; 22.39±9.5% vs 4.33±1.20%, P < 0.05). Compared with the normal control group and solvent control group, the exposure group had significantly decreased mRNA and protein expression of p53 and significantly increased mRNA and protein expression of cyclin E in BEAS-2B cells at passages 20 and 30 (P < 0.05).

CONCLUSIONCentrosome abnormalities occur before the malignant transformation in BEAS-2B cells treated with coal tar pitch smoke extracts, and they may be mediated by the p53/p21/cyclin E signaling pathway.

Cell Line ; Cell Transformation, Neoplastic ; metabolism ; pathology ; Centrosome ; metabolism ; pathology ; Coal Tar ; Cyclin E ; metabolism ; Epithelial Cells ; cytology ; metabolism ; Humans ; Signal Transduction ; Smoke ; Tumor Suppressor Protein p53 ; metabolism