Histology and histopathology Vol.18, nº 3 (2003)

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Browsing Histology and histopathology Vol.18, nº 3 (2003) by Subject "Angiogenesis"

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    Expression of hypoxia-inducible factor-1a (HIF-1a) in pituitary tumours
    (Murcia : F. Hernández, 2003) Vidal, S.; Horvath, E.; Kovacs, K.; Kuroki, T.; Lloyd, R.V.; Scheithauer, B.W.
    The present study was performed to investigate HIF-1a (hypoxia-inducible factor-1a) expression in a large number of immunohistochemically and ultrastructurally characterized surgically removed pituitary tumours. The potential relation of HIF-1a with outcome variables as well as the presence of HIF-1a expression in the tumours treated with dopamine agonists and octreotide, a long-acting somatostatin analogue was also investigated. HIF-1a immunoreactivity was confined to the nucleoplasm whereas the nucleoli were unconspicuous. The distribution of HIF-1a was evident in the tumours whereas normal adenohypophysial cells showed no HIF- 1a staining. HIF-1a expression was detected not only in the tumour cells but also in endothelial cells lining the blood vessels within the tumour. ACTH producing adenomas showed the lowest level of HIF-1a expression whereas pituitary carcinomas and GH producing adenomas had the highest counts. The statistical study demonstrated no significant correlation between HIF-1a expression, patient age, gender, tumour, size, invasiveness, cell proliferation rate and vascularity. These results suggest that the behaviour of pituitary tumours does not primarily depend of HIF-1a expression. Our study demonstrated an increase HIF-1a expression in bromocriptine treated PRL producing pituitary adenomas compared with untreated tumours but no increase in octreotide treated tumours.
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    Upregulation of vascular endothelial growth factor (VEGF) in the retinas of transgenic mice overexpressing interleukin-1ß (IL-1ß) in the lens and mice undergoing retinal degeneration
    (Murcia : F. Hernández, 2003) Vinores, S.A.; Xiao, W.H.; Zimmerman, R.; Whitcup, S.M.; Wawrousek, E.F.
    IL-1ß is a pro-inflammatory agent associated with angiogenesis and increased vascular permeability. To determine whether IL-1ß elicits these responses through an upregulation of VEGF, transgenic mice that overexpress IL-1ß in the lens were evaluated at various time points for the localization of VEGF, the location and extent of blood-retinal barrier (BRB) breakdown, and the origin and extent of neovascularization (NV). In homozygous and heterozygous transgenic mice, but not controls, intense VEGF immunoreactivity was scattered throughout the retina at postnatal days 5-7 (P5-7), just after the onset of inflammatory cell infiltration. VEGF staining in the retina remained widespread, but weak from P9-15. Beginning at P15, the intensity of VEGF immunoreactivity achieved a second peak, which it maintained through adulthood. This peak coincided with significant retinal destruction due to massive inflammation. The onset of BRB breakdown coincided with the upregulation of VEGF (P5-7) and widespread BRB breakdown was demonstrated from about P9. From P9-12, aggregates of cells positive for Griffonia simplicifolia isolectin-B4, a marker for vascular endothelial cells, formed on the retinal surface. These cells migrated into the retina at P12-15 with the more superficial cells forming a network of vessels and the deeper cells remaining in small clusters, thus demonstrating that NV occurs much later than BRB breakdown. Non-transgenic FVB/N mice, which undergo retinal degeneration beginning at about P9, also demonstrate the latter peak of VEGF upregulation and the accompanying BRB breakdown, but not the early upregulation. VEGF immunostaining of transgenic and non-transgenic mouse retinas was eliminated by preincubation of the VEGF antibodies with VEGF peptide. The data suggest that the early peak of VEGF upregulation (P5-7) and its accompanying BRB breakdown is due to IL-1ß expression and is likely to be dependent on inflammatory cell infiltration. The latter peak appears to be related to retinal destruction.