Histology and histopathology Vol.16, nº 3 (2001)
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- PublicationOpen AccessColonic endocrine cells in rats with chemically induced colon carcinoma(Murcia : F. Hernández, 2001) Sitohy, B.; El-Salhy, M.Colonic carcinoma was induced in male Sprague-Dawley rats by injecting them with 1,2- dimethylhydrazine dihydrochloride. Control rats were injected with EDTA solution. Tissue specimens of colon from four groups of animals: (i) rats without tumour, (ii) with dysplasia and lymphoid hyperplasia, (iii) with colonic adenocarcinoma, and (iv) controls, were investigated. The colonic endocrine cells were detected by immunocytochemistry and quantified by computerised image analysis. Peptide YY (PYY)- and serotonin-immunoreactive cells were found in the colon of al1 the groups investigated. There were few somatostatin- or enteroglucagon-immunoreactive cells and no pancreatic polypeptide (PP)-immunoreactive cells in the colon of any of the groups studied. The density of PYY-immunoreactive cells increased significantly in rats with dysplasia and lymphoid hyperplasia and in rats with colon carcinoma. There was no statistically significant difference as regards cell secretory index (CSI) or nuclear area of PYYimmunoreactive cells in any of treated groups examined. Nor was there any statistically significant difference between al1 treated animal groups and controls, as regards cell density, CSI, or nuclear area of serotoninimmunoreactive cells. The present observations in an animal model of human colon carcinoma support the assumption that neuroendocrine peptides in the gut are involved in the carcinogenesis of colorectal carcinoma. However, The nature of the changes in the colonic endocrine cells observed here differed from those in patients with colon carcinoma, possibly due to a difference between the response of young rats to an induced colon carcinoma and a spontaneously developed carcinoma in elderly humans, or due to a species difference.
- PublicationOpen AccessEffects of orexins A and B on the secretory and proliferative activity of immature and regenerating rat adrenal glands(Murcia : F. Hernández, 2001) Malendowicz, L.K.; Jedrzejczak, N.; Belloni, A. S.; Tretjer, M.; Hochol, A.; Nussdorfer, G.G.Orexins A and B are two hypothalamic peptides, involved in the central regulation of feeding, which act through two receptor subtypes, named OXIR and OX2R. OXIR is selective for orexin-A, and OX2R binds both orexins. We have investigated the effects of three subcutaneous injections of 10 nmollkg body weight of orexins on the secretion and proliferative activity of immature (20-day-old) and regenerating rat adrenal cortex. The presence of both OXIR and OX2R mRNAs has been detected by reverse transcriptionpolymerase chain reaction in adult, immature and regenerating adrenals. Orexin-A increased corticosterone plasma concentration in immature rats, but not in animals with regenerating adrenals. Both orexins raised metaphase index (%o of metaphase-arrested cells) in immature rat adrenals, orexin-B being more effective than orexin-A. In contrast, both orexins equipotently lowered adrenal metaphase index at day 5 (but not day 8) of adrenal regeneration. We conclude that orexins (1) stimulate secretion and proliferative activity of immature rat adrenals, acting through OXIR and OX2R, respectively; and (2) do not affect secretion, but inhibit proliferative activity of regenerating adrenals, mainly via the activation of OX2R.
- PublicationOpen AccessUltrastructural observations on the microvasculature in advanced gastric carcinomas(Murcia : F. Hernández, 2001) Caruso, R.A.; Speciale, G.; Inferrera, A.; Rigolis, L.; Inferrera, C.The ultrastructural features associated with vascular permeability in 9 cases of advanced gastric carcinomas were studied, and compared with that of control non-neoplastic mucosa. Tumour rnicrovasculature showed features in common with those of control mucosa, including complete basa1 lamina, welldeveloped interendothelial junctions, fenestrations and caveolae. Some tumour blood vessels showed endothelial cell swelling accompained by luminal narrowing and perivascular fibrosis. In 2 out of 9 cases, there were endothelial attenuation with numerous fenestrations and vesiculo-vacuolar organelles. The vesiculo-vacuolar organelle is a recently described cytoplasmic structure found in the endothelial cells lining turnour microvessels and normal venules and which provides an important pathway for extravasation of circulating macromolecules. Our ultrastructural data suggest that advanced gastric carcinomas share with experimental tumour models in vivo only some morphologic features associated with hyperpermeability including fenestration, endothelial attenuation and vesiculo-vacuolar organelles. The implications of perivascular fibrosis on the delivery of immune cells to gastric carcinomas are discussed.
- PublicationOpen AccessPotential role of a new anti-03 integrin antibody in the development of intimal hyperplasia after vascular surgery: an in vitro smooth muscle cell model(Murcia : F. Hernández, 2001) Gimeno, M.J.; González, J.; Rodríguez, M.; Corrales, C.; Bellón, J.M.; Buján, J.The occurrence of intimal hyperplasia after vascular surgery is an ongoing concern in current clinical practice. Arnong the many factors involved in the development of this pathology, platelet adhesion and myointimal proliferation play a major role. Both these processes are mediated by integrins (mainly avP3 integrins). Over the past years, severa1 substances have been designed to delay or inhibit the cell proliferation that leads to hyperplasia and mainly include monoclonal antibodies directed against integrins. The aim of the present study was to evaluate the effects of an antibody denoted P37 (anti B3 integrin) on human smooth muscle cells (SMC) and its role in blocking the 83 subunit. To this end, SMC from human umbilical artery were cultured in the presence or absence of the cell substrate vitronectin (VN) and incubated with P37. After 4 days of treatment, determination was made of cell proliferation and migration. Smooth muscle cells grown on VN showed increased proliferation and migration compared to control VN-free cultures. However, the presence of P37 in the culture medium inhibited proliferation and reduced migration. Combined treatment with VN and P37 led to improved proliferation but VN was unable to reverse the effects on migration observed in the former cultures. Results suggest that in vitro, P37 is capable of blocking human SMC 83 integrins and thus impedes cell proliferation and migration These findings may have clinical implications related to modulation of the development of hyperplasia.
- PublicationOpen AccessCellular and molecular basis of fibrous dysplasia(Murcia : F. Hernández, 2001) Marie, P.J.Recent advances have been made in the cellular and molecular mechanisms involved in monostotic and polyostotic fibrous dysplasia, a rare nonmalignant disease causing bone deformations and fractures. The molecular basis of fibrous dysplasia has been clarified when mutations affecting the stimulatory a subunit of G protein (Gs) have been found in dysplastic bone lesions. The histological analysis of dysplastic lesions revealed that the mutations in Gsa caused abnormalities in cells of the osteoblastic lineage and therefore in the bone matrix. Further in vitro analyses of bone cells from mutant dysplastic bone lesions revealed that the abnormal deposition of immature bone matrix in fibrous dysplasia results from decreased differentiation and increased proliferation of osteoblastic cells. Finally, the signaling pathway involved in these osteoblastic abnormalities has been identified. It is now apparent that the constitutive elevation in cAMP leve1 induced by the Gsa mutations leads to alterations in the expression of several target genes whose promoters contain cAMP-responsive elements, such as c-fos, c-jun, 11-6 and 11-11. This in turn affects the transcription and expression of downstream genes and results in the alterations of osteoblast recruitment and function in dysplastic bone lesions. These mechanisms provide a cellular and molecular basis for the alterations in bone cells and bone matrix in fibrous dysplasia.