No abstract available.
Animals ; Epidermal Growth Factor* ; Mesangial Cells* ; Rats*

No abstract available.
Adenocarcinoma* ; Carcinoma, Squamous Cell* ; Epidermal Growth Factor* ; Epithelial Cells* ; Lung* ; Receptor, Epidermal Growth Factor*

Mucus hypersecretion is a common response to chronic inflammation in the lower airways and is a hallmark of chronic rhinosinusitis. It contributes to their morbidity and mortality by plugging airways and causing recurrent infections in lower airway. At present there is no specific treatment for mucus hypersecretion. However, it has been discovered that epithelial growth factor receptor (EGFR) expression and activation causes mucin production in airways. An EGFR pathway is implicated in mucus cell differentiation induced by various stimuli; therefore, inhibition of the EGFR transduction cascade may provide effective new treatments for hypersecretory airway diseases. EGFR pathways have also been implicated in the regranulation of goblet cell in the airway epithelium. Proving this theory will require the use of selective EGFR inhibitors in clinical studies of nasal hypersecretory states.
Cell Differentiation ; Epidermal Growth Factor* ; Epithelium* ; Goblet Cells ; Inflammation ; Mortality ; Mucins* ; Mucus ; Receptor, Epidermal Growth Factor*

BACKGROUND: We investigated whether wogonin and apigenin significantly affect the epidermal growth factor receptor (EGFR) signaling pathway involved in MUC5AC mucin gene expression, and production from cultured airway epithelial cells; this was based on our previous report that apigenin and wogonin suppressed MUC5AC mucin gene expression and production from human airway epithelial cells. METHODS: Confluent NCI-H292 cells were pretreated with wogonin or apigenin for 15 minutes or 24 hours and then stimulated with epidermal growth factor (EGF) for 24 hours or the indicated periods. RESULTS: We found that incubation of NCI-H292 cells with wogonin or apigenin inhibited the phosphorylation of EGFR. The downstream signals of EGFR such as phosphorylation of MEK1/2 and ERK1/2 were also inhibited by wogonin or apigenin. CONCLUSION: The results suggest that wogonin and apigenin inhibits EGFR signaling pathway, which may explain how they inhibit MUC5AC mucin gene expression and production induced by EGF.
Apigenin* ; Epidermal Growth Factor* ; Epithelial Cells* ; Gene Expression* ; Humans ; Mucins* ; Phosphorylation ; Receptor, Epidermal Growth Factor*

No abstract available.
Carcinoma, Squamous Cell ; Epidermal Cyst ; Epithelial Cells ; Ulcer

Schwannomas of the sinonasal tract are very rare benign neoplasm, which can arise from nerve sheath containing Schwann cells. Epidermal cysts are also rarely present in nasal cavity. They are thought to be congenital lesion associated with various craniofacial disorders or arise as a result of implantation of epidermal cells into the deeper dermal element. Several cases of the nasal schwannoma or epidermal cyst have been reported repectively, however nasal schwannoma with epidermal cyst never has been reported yet. We report the first case of nasal schwannoma which is coexists with epidermal cyst at the superior turbinate of the nasal cavity.
Epidermal Cyst* ; Nasal Cavity ; Neurilemmoma* ; Schwann Cells ; Turbinates

Objective: To investigate the regulatory effects of bio-intensity electric field on directional migration and microtubule acetylation in human epidermal cell line HaCaT, aiming to provide molecular theoretical basis for the clinical treatment of wound repair. Methods: The experimental research methods were used. HaCaT cells were collected and divided into simulated electric field group (n=54) placed in the electric field device without electricity for 3 h and electric field treatment group (n=52) treated with 200 mV/mm electric field for 3 h (the same treatment methods below). The cell movement direction was observed in the living cell workstation and the movement velocity, trajectory velocity, and direction of cosθ of cell movement within 3 h of treatment were calculated. HaCaT cells were divided into simulated electric field group and electric field treatment 1 h group, electric field treatment 2 h group, and electric field treatment 3 h group which were treated with 200 mV/mm electric field for corresponding time. HaCaT cells were divided into simulated electric field group and 100 mV/mm electric field group, 200 mV/mm electric field group, and 300 mV/mm electric field group treated with electric field of corresponding intensities for 3 h. The protein expression of acetylated α-tubulin was detected by Western blotting (n=3). HaCaT cells were divided into simulated electric field group and electric field treatment group, and the protein expression of acetylated α-tubulin was detected and located by immunofluorescence method (n=3). Data were statistically analyzed with Kruskal-Wallis H test,Mann-Whitney U test, Bonferroni correction, one-way analysis of variance, least significant difference test, and independent sample t test. Results: Within 3 h of treatment, compared with that in simulated electric field group, the cells in electric field treatment group had obvious tendency to move directionally, the movement velocity and trajectory velocity were increased significantly (with Z values of -8.53 and -2.05, respectively, P<0.05 or P<0.01), and the directionality was significantly enhanced (Z=-8.65, P<0.01). Compared with (0.80±0.14) in simulated electric field group, the protein expressions of acetylated α-tubulin in electric field treatment 1 h group (1.50±0.08) and electric field treatment 2 h group (1.89±0.06) were not changed obviously (P>0.05), while the protein expression of acetylated α-tubulin of cells in electric field treatment 3 h group (3.37±0.36) was increased significantly (Z=-3.06, P<0.05). After treatment for 3 h, the protein expressions of acetylated α-tubulin of cells in 100 mV/mm electric field group, 200 mV/mm electric field group, and 300 mV/mm electric field group were 1.63±0.05, 2.24±0.08, and 2.00±0.13, respectively, which were significantly more than 0.95±0.27 in simulated electric field group (P<0.01). Compared with that in 100 mV/mm electric field group, the protein expressions of acetylated α-tubulin in 200 mV/mm electric field group and 300 mV/mm electric field group were increased significantly (P<0.01); the protein expression of acetylated α-tubulin of cells in 300 mV/mm electric field group was significantly lower than that in 200 mV/mm electric field group (P<0.05). After treatment for 3 h, compared with that in simulated electric field group, the acetylated α-tubulin of cells had enhanced directional distribution and higher protein expression (t=5.78, P<0.01). Conclusions: Bio-intensity electric field can induce the directional migration of HaCaT cells and obviously up-regulate the level of α-ubulin acetylation after treatment at 200 mV/mm bio-intensity electric field for 3 h.
Humans ; Acetylation ; Tubulin/metabolism* ; Microtubules/metabolism* ; Electricity ; Epidermal Cells/metabolism*

Epidermoid cysts are generally benign neoplastic lesions, the etiology of which is unclear and is mainly related to epithelial cells left in the tissues during the embryonic period and traumatically implanted in the tissues. The most common intraosseous sites are the phalanges and the skull. Epidermoid cysts occurring in the jaws are clinically rare. In this paper, we report a case of epidermoid cyst occurring in the mandible with embedded teeth and discuss the etiology, clinical manifestations, diagnosis, and treatment of epidermoid cysts in the jaws in the context of the relevant literature.
Humans ; Epidermal Cyst/surgery* ; Skull ; Mandible ; Diagnosis, Differential ; Epithelial Cells

Growth stimulatory/inhibitory factors and their receptors are the important mediators of control of epithelial cell proliferation and differentiation. The aim of this study was to observe the distribution of epidermal growth factor receptor (EGFR) and transforming growth factor-beta1 type II receptor (TbetaRII) during carcinogenesis of oral squamous cell carcinoma (OSCC). Formalin fixed, paraffin embedded tissue from 25 oral leukoplakias (OL) and 15 OSCC was immunostained by avidin-biotin complex method. In OSCC, the carcinomatous area and the adjacent dysplastic/ hyperplastic area were examined. In OL, the hyperplasia and the epithelial dysplasia were examined. Monoclonal anti-EGFR Ab and polyclonal anti-TbetaRII Ab were applied. EGFR was mainly expressed in the basal layer and was increased with epithelial dysplasia in OL. TbetaRII was not detected in the basal cell layer and dysplastic area in OL. In contrast, the dysplastic area adjacent to OSCC showed positivity in the entire layer including the dysplastic area. In all cases of OSCC, both EGFR and TbetaRII showed positive reactions. EGFR was increased with the progression to the malignancy, and the expression pattern of TbetaR II was altered to be positive in the basal cell layer with progression to malignancy. These results suggest that the expression of EGFR appeared to be an early event and TbetaR II may be related to malignant transformation during oral carcinogenesis. The expression pattern of EGFR and TbetaR II may contribute to predict the risk of the development of carcinoma in oral premalignant lesions.
Carcinogenesis ; Carcinoma, Squamous Cell* ; Epidermal Growth Factor* ; Epithelial Cells ; Formaldehyde ; Hyperplasia ; Leukoplakia, Oral* ; Paraffin ; Receptor, Epidermal Growth Factor*

BACKGROUND: The overexpression of epidermal growth factor receptor (EGFR) and c-erbB-2 oncogenes has been implicated in the development of many types of cancer. However, the role of EGFR and c-erbB-2 overexpression in hepatocellular carcinoma (HCC) has not been fully elucidated. METHODS: The aim of this study was to evaluate the immunohistochemical expression of EGFR and c-erbB-2 oncoprotein in a series of 52 HCCs. RESULTS: All but one of the HCC tumor tissues were negative for EGFR monoclonal antibody, clone H11. All of the HCC tumor tissue samples were negative for EGFR monoclonal antibody, clone 29.1.1. However, strong EGFR immunoreactivity was detected in sinusoidal endothelial cells of HCC in 25 tumors (48%) using EGFR 29.1.1 antibody. The expression of c-erbB-2 was observed in 6% (3/52) of the HCCs. No significant correlation was found between p53 mutation and the expression of c-erbB-2. CONCLUSION: Our results suggest that both EGFR and c-erbB-2 oncoprotein overexpressions in tumor cells are rare and do not seem to predominantly contribute to the malignant phenotype in HCC.
Carcinoma, Hepatocellular* ; Clone Cells ; Endothelial Cells ; Oncogenes ; Phenotype ; Receptor, Epidermal Growth Factor