Skin wound healing is a complex event, and interrupted wound healing process could lead to scar formation. The aim of this study was to examine the morphological changes of scar tissue. Pathological staining (HE staining, Masson's trichrome staining, methenamine silver staining) was used to evaluate the morphological changes of regenerating epidermis in normal skin and scar tissue, and immunofluorescence staining to detect the expression of collagen IV, a component of basement membrane (BM), and the expression of integrinβ4, a receptor for BM laminins. Additionally, the expression of CK14, CK5, and CK10 was measured to evaluate the proliferation and differentiation of keratinocytes in normal skin and scar tissue. The results showed that the structure of the skin was histologically changed in scar tissue. Collagen IV, expressed under the epidermis of normal skin, was reduced distinctly in scar tissue. Integrinβ4, expressed in the basal layer of normal skin, was found absent in the basal layer of scar tissue. Additionally, it was found that keratinocytes in scarring epidermis were more proliferative than in normal skin. These results indicate that during the skin wound healing, altered formation of BM may affect the proliferation of keratinocytes, reepithelial and tissue remodeling, and then result in scar formation. Thus, remodeling BM structure during wound repair may be beneficial for improving healing in cutaneous wounds during clinical practice.
Adolescent ; Adult ; Cicatrix ; metabolism ; pathology ; Collagen Type IV ; metabolism ; Female ; Humans ; Integrin beta4 ; metabolism ; Keratinocytes ; cytology ; metabolism ; pathology ; Male ; Skin ; cytology ; metabolism ; pathology

To explore the relationship between the epithelial adhesion molecules and immune responses of airway epithelium, we observed the expression of integrin β4 and intercellular adhesion molecule-1 (ICAM-1) in the mice airway epithelium after sensitization with allergens. BALB/c mice were sensitized with intraperitoneal injection of ovalbumin (OVA) or house dust mite (HDM) and then developed airway hyper-responsiveness as determined by barometric whole-body plethysmography. Both OVA and HDM sensitization led to increases of the number of peripheral leukocytes as well as inflammatory cells infiltration in lungs. OVA sensitized mice showed more severe inflammatory cells infiltration than HDM sensitized mice. Immunohistochemistry analysis of mice lung tissues revealed that sensitization with both allergens also led to a decrease of integrin β4 expression and an increase of ICAM-1 expression in airway epithelia. OVA sensitized mice showed a more significant increase of ICAM-1 expression compared with HDM sensitized mice. siRNA mediated silencing of integrin β4 gene in 16HBE cells resulted in an up-regulation of ICAM-1 expression. Our results indicate a possible role of airway epithelial adhesion molecules in allergen-induced airway immune responses.
Allergens ; pharmacology ; Animals ; Integrin beta4 ; metabolism ; Intercellular Adhesion Molecule-1 ; metabolism ; Lung ; metabolism ; physiopathology ; Mice ; Mice, Inbred BALB C ; Ovalbumin ; Pyroglyphidae ; Respiratory Hypersensitivity ; metabolism

BACKGROUND AND OBJECTIVES: Retinoids have been used in chemoprevention trials for a variety of epithelial malignancies. However, high incidence of toxicity and drug resistance remains as problems. Increase of the retinoid metabolism by cytochrome P450 has been known as one of the several mechanisms explaining these toxicity and the aquired resistance. There have been many studies about the biological effects of retinoids in head and neck squamous cell carcinoma (HNSCC), but there is no information about the effects of the retinoids metabolism on cell biology. The study presented here is designed to examine the relationship between cytochrome P450 induction and responses to retinoids in the HNSCC cell lines. MATERIAL AND METHODS: We used a human HNSCC cell lines (AMC-HN-4, AMC-HN-6). The change of metabolic activity was analyzed using thin layer chromatography (TLC). The effects of retinoids on cell proliferation were evaluated with CellTiter 96 TMAQueous Cell Proliferation Assay. The effects of retinoids on beta4 integrin expression were evaluated with flow cytometry. RESULTS: The inhibitory effects of retinoids on cell proliferation were higher in AMC-HN-4 cell line (cytochrome P450 uninducible) than in AMC-HN-6 cell line (cytochrome P450 inducible) (p<0.05). The expression of beta4 integrin was more effectively suppressed in the AMC-HN-4 cell line than in the AMC-HN-6 cell line. CONCLUSION: The results of this study suggest that cytochrome P450 inducilbility may be an important factor to determine the biological effects of retinoids in HNSCC cells.
Carcinoma, Squamous Cell* ; Cell Line* ; Cell Proliferation ; Chemoprevention ; Chromatography, Thin Layer ; Cytochrome P-450 Enzyme System ; Drug Resistance ; Flow Cytometry ; Head* ; Humans ; Incidence ; Integrin beta4* ; Metabolism ; Neck* ; Retinoids*

Vertically aligned, laterally spaced nanoscale titanium nanotubes were grown on a titanium surface by anodization, and the growth of chondroprogenitors on the resulting surfaces was investigated. Surfaces bearing nanotubes of 70 to 100 nm in diameter were found to trigger the morphological transition to a cortical actin pattern and rounded cell shape (both indicative of chondrocytic differentiation), as well as the up-regulation of type II collagen and integrin beta4 protein expression through the down-regulation of Erk activity. Inhibition of Erk signaling reduced stress fiber formation and induced the transition to the cortical actin pattern in cells cultured on 30-nm-diameter nanotubes, which maintained their fibroblastoid morphologies in the absence of Erk inhibition. Collectively, these results indicate that a titanium-based nanotube surface can support chondrocytic functions among chondroprogenitors, and may therefore be useful for future cartilaginous applications.
Animals ; Apoptosis ; Cell Differentiation/*drug effects ; Cells, Cultured ; Chick Embryo ; Chickens ; Chondrocytes/cytology/drug effects/metabolism ; Chondrogenesis/*drug effects ; Collagen Type II/metabolism ; Immunohistochemistry ; Integrin beta4/metabolism ; Mesenchymal Stem Cells/*cytology/*drug effects/metabolism ; Nanotubes/*chemistry ; Titanium/*chemistry/*pharmacology