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The localisation of oestrogen (ER) and epidermal growth factor receptors (EGFR) in the various cell types of the bitch uterine was determined. In this study, 23 adult, healthy crossbred bitches brought to the clinic for ovariohisterectomy were used. ER and EGFR positive staining was detected in all cell types of the uterus. A distinct staining was seen in the luminal and glandular epithelium; while stromal and myometrial cells showed weak or moderate staining. The endothelial and smooth muscle cells of the vessels in the endometrium and myometrium sometimes appeared positive. No staining was observed in the mesothelium. The results of this study suggested that ER and EGFR were expressed at various levels in different cell types of bitch uterus. In light of the previous studies, and data of the presented investigations, it may be necesssary to elicit the harmonious proliferation and differentiation of epithelial and stromal cells that are considered essential for the preparation of the uterus for implantation.
The aim of the study was to determine the potential prognostic significance of intratumoral microvessel density assessment with panendothelial marker CD34, a new and specific marker for new blood microvessels CD 105, and a potent angiogenesis modulator, epidermal growth factor receptor (EGF-R) expression in women with serous ovarian cancer. Our results suggest that strong expression of EGF-R may be a prognostic of prognostic value in women operated because of serous cancer of ovaries.
The aim of this study was to investigate whether transforming growth factor-β1 (TGF-β1) could induce alveolar epithelial-mesenchymal transition (EMT) in vitro, and whether Smad7 gene transfer could block this transition. We also aimed to elucidate the possible mechanisms of these processes. The Smad7 gene was transfected to the rat type II alveolar epithelial cell line (RLE-6TN). Expression of the EMT-associated markers was assayed by Western Blot and Real-time PCR. Morphological alterations were examined via phase-contrast microscope and fluorescence microscope, while ultrastructural changes were examined via electron microscope. TGF-β1 treatment induced a fibrotic phenotype of RLE-6TN with increased expression of fibronectin (FN), α-smooth muscle actin (α-SMA) and vimentin, and decreased expression of E-cadherin (E-cad) and cytokeratin19 (CK19). After transfecting the RLE-6TN with the Smad7 gene, the expression of the mesenchymal markers was downregulated while that of the epithelial markers was upregulated. TGF-β1 treatment for 48 h resulted in the separation of RLE-6TN from one another and a change into elongated, myofibroblast-like cells. After the RLE-6TN had been transfected with the Smad7 gene, TGF-β1 treatment had no effect on the morphology of the RLE-6TN. TGF-β1 treatment for 48 h resulted in an abundant expression of α-SMA in the RLE-6TN. If the RLE-6TN were transfected with the Smad7 gene, TGF-β1 treatment for 48 h could only induce a low level of α-SMA expression. Furthermore, TGF-β1 treatment for 12 h resulted in the degeneration and swelling of the osmiophilic multilamellar bodies, which were the markers of type II alveolar epithelial cells. TGF-β1 can induce alveolar epithelialmesenchymal transition in vitro, which is dependent on the Smads signaling pathway to a certain extent. Overexpression of the Smad7 gene can partially block this process.
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