ABSTRACT
Objective To explore the correlation of the formation of pseudoepitheliomatous hyperplasia (PEH) after healing of inappropriately treated wound of skin with epithelial mesenchymal cells transdifferentiation (EMT). Methods Morphological change in epithelial tissue was observed with histopathologic methods in epithelial cells from PEH lesions ( n =11) and normal skin specimens obtained adjacent to PEH (PEH N, n =6) from 11 patients with PEH. At the same time, the characteristic of expressions and distribution of type Ⅰ and Ⅲ collagen, alpha smooth muscule actin (? SMA), vimentin (Vim), desmin (Des), transforming growth factor ?1 (TGF ?1)and its receptor (TGFRI), pan cytokeratin (CKp), and type Ⅳ collagen in PEH were examined with indirect immunofluorescent double labelling method. Results In comparison with PEH N, squamous epithelium in PEH presented a picture of atypical hyperplasia, there was a derangement of basal apical polarity, disrupture in structure, and a displacement of cells foward mesenchyme. Examination under electron microscope revealed deformation of epithelial basal cells, with loose intercellular junction, and newly formed tumor like cells distingaishable from original epithelial cells. Expressions of type Ⅰ and Ⅲ collagen,? SMA,Vim and Des could be detected in the epithelial cells of PEH. However,the protein expressions of CKp, Ⅳ type collagen were significantly decreased in basal epithelial cells. Furthermore, free epithelial cells expressing CKp were found in the deep layer of mesenchyme. Conclusion It was confirmed for the first time that there was a phenomenon of EMT during the course of PEH formation. Epithelial cells in PEH lesion with granuloma and non hypertrophic scar are characteristized by de differentiation, redifferentiation and a decrement of TGF ?1 induction, which are involved in reactive hyperplasia of the epithelium.
ABSTRACT
Objective To investigate the changes of the activity and the distribution of the rat cardiac calcineurin (CaN) which is the signalling molecule of the hypertrophy induced by the external aldosterone(Ald), and to detect the mechanism of the regulation of CaN. Methods 21 male wister rats were randomly divided into 3 groups: group Ald(7 rats), treated with Ald 18?g/d, peritoneal injection (i p) for 4 weeks; group spironolactone (spiron) (7 rats), treated with Ald and with spiron 20mg?kg -1 ?d -1 oral for 4 weeks; and group control (7 rats). The plasma concentrations of Ald, angiotensin Ⅱ(Ang Ⅱ)and endothelin(ET), blood levels of NO, the tissue activity of the CaN and distribution of CaN A? in the myocardium of the left ventricle, were detected in the rats by the radioimmunoassay , by the nitrate assay, by the chromophoric assay and by the immunohistochemistry, respectively. Results The concentration of the plasma Ald increased by 1 62 times, the blood NO - 3 concentration was deceased, the ratio of Ald over NO - 3( Ald/ NO - 3) increased by 2 95 times, and the cardiac tissue levels of CaN activity was were 1 47 times higher, in the rats treated with ald than in the normotensive rats. CaN A? distributed over cardiac cytoplasm, and the positive dyeing of the local CaN A? in the cytoplasm was thick near the cell membrane in the rats treated with Ald. The treatment with spiron could decreased the blood levels of the AngII?Ald/ NO - 3?ET/NO - 3?AngII/ NO - 3 and the tissue activity of myocardial CaN, positive dyeing of the local CaN A? in the cytoplasm, and increased blood NO - 3 concentration. Conclusion The aldosterone may be the main stimuli factor which can damage the balance of the blood active factors, and then make a novel cardiac hypertrophic signalling molecule calcineurin activated and redistributed in the cytoplasm of the rat left ventricular myocardium