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- W1818490247 abstract "The role of members of the Vascular Endothelial Growth Factor (VEGF) family and their receptors in angiogenesis, progression and pathophysiology of pituitary tumours is still poorly understood. In the present work, the expression and localization of the angiogenic factor VEGF-A and the lymphangiogenic factor VEGF-C, as well as VEGF receptors (VEGFR-1, VEGFR-2, VEGFR-3 and neuropilin-1), have been studied in normal and tumoural pituitary tissue and in transformed pituitary tumour cell lines. In addition, the role and mechanism of action of VEGFR-1 ligands have been investigated in normal and transformed rat pituitary cells. Immunohistochemical investigations in 3 normal human adenohypophyses showed that VEGFR-2 and neuropilin-1 were localized in blood vessel endothelial cells, while VEGFR-1 was found in endocrine cells. VEGF-A significantly induced ACTH and prolactin secretion in normal rat pituitary cell cultures, indicating a role of VEGF-A and VEGFR-1 in the regulation of the secretion of these pituitary hormones. In contrast, VEGFR-2 and its co-receptor neuropilin-1 may be needed to maintain optimal intrapituitary vascularization and blood vessel permeability. Although no lymphatic vessels were identified in normal adenohypophysis, the lymphangiogenic factor VEGF-C and its receptor VEGFR-3 were detected by immunohistochemistry, suggesting the involvement of the VEGF-C/VEGFR-3 system, usually implicated in lymphangiogenesis, in the maintenance of blood vessel permeability. The expression of VEGFR-1, VEGFR-2 and neuropilin-1 in a series of 39 pituitary adenomas reflected the same immunohistochemical localization pattern as observed in the normal adenohypophysis tissue. It was highly heterogeneous and mostly no significant correlation with different parameters, such as: tumour type, tumour grade, proliferation index (PI) and blood vessel number, was noticed. Only the absence of VEGFR-2 and neuropilin-1 correlated with a low PI, suggesting a role of these two receptors in increasing vessel permeability and consequently the availability of nutrients and oxygen for tumour cells. Functional studies, with the VEGFR-1-positive somatotrophinoma rat pituitary cell line MtT-S, showed that VEGF-A and the VEGFR-1 specific ligand PlGF, significantly stimulated the cell proliferation, through the activation of PI3K pathway and the induction of the anti-apoptotic factor Bcl-2 and the cell cycle promoter cyclin D1.VEGF-C immunostaining was detected in endocrine tumour cells of 10 adenomas and VEGFR-3 immunopositive vessels were found in 22 tumours, even if only 9 of them were positive for both VEGFR-3 and LYVE-1 (specific lymphatic vessel marker), suggesting that the VEGF-C/VEGFR-3 system may have a role in the regulation of tumour angiogenesis of pituitary adenomas, rather than in lymphangiogenesis, as already shown in other tumour types. In conclusion, the results of the present study provide strong evidence that VEGF may not only have a role in regulating pituitary adenoma neovascularization but also, through VEGFR-1, may affect pituitary adenoma pathophysiology by modulating growth, cell cycle progression and survival of the adenoma cells." @default.
- W1818490247 created "2016-06-24" @default.
- W1818490247 creator A5054075254 @default.
- W1818490247 date "2006-04-05" @default.
- W1818490247 modified "2023-09-26" @default.
- W1818490247 title "Localization and functional study of VEGF receptors in normal and adenomatous pituitary: evidence for a non-angiogenic role of VEGF" @default.
- W1818490247 cites W1044883788 @default.
- W1818490247 cites W11889541 @default.
- W1818490247 cites W124555615 @default.
- W1818490247 cites W1482045472 @default.
- W1818490247 cites W1482426502 @default.
- W1818490247 cites W1509669696 @default.
- W1818490247 cites W1516154474 @default.
- W1818490247 cites W1529396499 @default.
- W1818490247 cites W1549834656 @default.
- W1818490247 cites W1549893543 @default.
- W1818490247 cites W1552528612 @default.
- W1818490247 cites W1570971207 @default.
- W1818490247 cites W1582316077 @default.
- W1818490247 cites W1583777607 @default.
- W1818490247 cites W1586129343 @default.
- W1818490247 cites W1587020653 @default.
- W1818490247 cites W1591057067 @default.
- W1818490247 cites W1600542667 @default.
- W1818490247 cites W1601632081 @default.
- W1818490247 cites W163448755 @default.
- W1818490247 cites W1636539495 @default.
- W1818490247 cites W1639582946 @default.
- W1818490247 cites W1679229092 @default.
- W1818490247 cites W172183759 @default.
- W1818490247 cites W1726025741 @default.
- W1818490247 cites W1813183121 @default.
- W1818490247 cites W1826880678 @default.
- W1818490247 cites W1837651204 @default.
- W1818490247 cites W1875554126 @default.
- W1818490247 cites W1879346051 @default.
- W1818490247 cites W1889842940 @default.
- W1818490247 cites W1905816499 @default.
- W1818490247 cites W1930719228 @default.
- W1818490247 cites W1963876488 @default.
- W1818490247 cites W1964429954 @default.
- W1818490247 cites W1964455098 @default.
- W1818490247 cites W1964533512 @default.
- W1818490247 cites W1964951841 @default.
- W1818490247 cites W1965912140 @default.
- W1818490247 cites W1966535797 @default.
- W1818490247 cites W1967114357 @default.
- W1818490247 cites W1967244268 @default.
- W1818490247 cites W1967450352 @default.
- W1818490247 cites W1968781270 @default.
- W1818490247 cites W1969304986 @default.
- W1818490247 cites W1969939692 @default.
- W1818490247 cites W1972438151 @default.
- W1818490247 cites W1974165456 @default.
- W1818490247 cites W1974190969 @default.
- W1818490247 cites W1975290731 @default.
- W1818490247 cites W1975304932 @default.
- W1818490247 cites W1977980079 @default.
- W1818490247 cites W1980969801 @default.
- W1818490247 cites W1981612052 @default.
- W1818490247 cites W1983109837 @default.
- W1818490247 cites W1983763042 @default.
- W1818490247 cites W1984418041 @default.
- W1818490247 cites W1985804036 @default.
- W1818490247 cites W1985844240 @default.
- W1818490247 cites W1987268488 @default.
- W1818490247 cites W1988106051 @default.
- W1818490247 cites W1988835053 @default.
- W1818490247 cites W1991942906 @default.
- W1818490247 cites W1991958278 @default.
- W1818490247 cites W1995658890 @default.
- W1818490247 cites W1996320905 @default.
- W1818490247 cites W1996695017 @default.
- W1818490247 cites W1997700797 @default.
- W1818490247 cites W1999012962 @default.
- W1818490247 cites W1999330214 @default.
- W1818490247 cites W1999647970 @default.
- W1818490247 cites W2000292756 @default.
- W1818490247 cites W2000780971 @default.
- W1818490247 cites W2000953895 @default.
- W1818490247 cites W2001298205 @default.
- W1818490247 cites W2003964084 @default.
- W1818490247 cites W2004456466 @default.
- W1818490247 cites W2006644254 @default.
- W1818490247 cites W2007667671 @default.
- W1818490247 cites W2008509494 @default.
- W1818490247 cites W2008720144 @default.
- W1818490247 cites W2009946316 @default.
- W1818490247 cites W2010468452 @default.
- W1818490247 cites W2010972042 @default.
- W1818490247 cites W2011268436 @default.
- W1818490247 cites W2011314273 @default.
- W1818490247 cites W2011403734 @default.
- W1818490247 cites W2011723510 @default.
- W1818490247 cites W2013730676 @default.
- W1818490247 cites W2014148719 @default.
- W1818490247 cites W2014943535 @default.
- W1818490247 cites W2015344488 @default.
- W1818490247 cites W2022950801 @default.
- W1818490247 cites W2023052504 @default.