Expression of CD44, Vascular Endothelial Growth Factor, and Proliferating Cell Nuclear Antigen in Severe Venous Invasional Colorectal Cancer and Its Relationship to Liver Metastasis

Surgery Today ◽  
2000 ◽  
Vol 30 (4) ◽  
pp. 323-327 ◽  
Author(s):  
Yoshiaki Sumiyoshi ◽  
Yuichi Yamashita ◽  
Takafumi Maekawa ◽  
Norimi Sakai ◽  
Takayuki Shirakusa ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Liver Metastasis ◽  
Proliferating Cell Nuclear Antigen ◽  
Nuclear Antigen ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor ◽  
Proliferating Cell

scholarly journals Activated Microvessels Express Vascular Endothelial Growth Factor and Integrin αvβ3 During Focal Cerebral Ischemia

1999 ◽  
Vol 19 (9) ◽  
pp. 1038-1050 ◽  
Author(s):  
Takeo Abumiya ◽  
Jacinta Lucero ◽  
Ji Hoe Heo ◽  
Masafumi Tagaya ◽  
James A. Koziol ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Proliferating Cell Nuclear Antigen ◽  
Focal Cerebral Ischemia ◽  
Integrin Αvβ3 ◽  
Nuclear Antigen ◽  
Vascular Endothelial ◽  
Primate Model ◽  
Endothelial Growth Factor ◽  
Proliferating Cell

Both vascular endothelial growth factor (VEGF) and integrin αvβ3 play roles in angiogenesis. In noncerebral vascular systems, VEGF can induce endothelial integrin αvβ3 expression. However, it is unknown whether VEGF, like integrin αvβ3, appears in the initial response of microvessels to focal brain ischemia. Their coordinate expression in microvessels of the basal ganglia after middle cerebral artery occlusion (MCAO) in the nonhuman primate model was examined quantitatively. Cells incorporating deoxyuridine triphosphate (dUTP+) by the polymerase I reaction at 1 hour (n = 3), 2 hours (n = 3), and 7 days (n = 4) after MCAO defined the ischemic core (Ic) and peripheral regions. Both VEGF and integrin αvβ3 were expressed by activated noncapillary (7.5- to 30.0-μm diameter) microvessels in the Ic region at 1 and 2 hours after MCAO. At 7 days after MCAO, the number of VEGF+, integrin αvβ3+, or proliferating cell nuclear antigen-positive microvessels had decreased within the Ic region. The expressions of VEGF, integrin αvβ3, and proliferating cell nuclear antigen were highly correlated on the same microvessels using hierarchical log-linear statistical models. Also, VEGF and subunit αv messenger ribonucleic acids were coexpressed on selected microvessels. Here, noncapillary microvessels are activated specifically early during a focal cerebral ischemic insult and rapidly express VEGF and integrin αvβ3 together.

scholarly journals Autocrine/Paracrine Action of Pituitary Vasoactive Intestinal Peptide on Lactotroph Hyperplasia Induced by Estrogen

Endocrinology ◽  
2003 ◽  
Vol 144 (10) ◽  
pp. 4403-4409 ◽  
Author(s):  
Oscar Gómez ◽  
José Antonio Balsa
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Receptor Antagonist ◽  
Proliferating Cell Nuclear Antigen ◽  
Nuclear Antigen ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor ◽  
Proliferating Cell ◽  
Tgf Β1 ◽  
Vip Receptor

Vasoactive intestinal polypeptide (VIP) content is increased in the hyperplastic pituitaries of estrogen (E)-treated rats, thus suggesting that this neuropeptide could mediate the E effect on lactotrophs. E also decreases pituitary TGF-β1 content, an autocrine/paracrine inhibitor of lactotroph proliferation, and induces pituitary angiogenesis. To elucidate the role of VIP in this context, lactotroph hyperplasia was induced in female Fisher 344 rats by implanting sc pellets of diethylstilbestrol (DES). Twenty-five days later, the rats were treated with three different increasing doses of a VIP receptor antagonist or the vehicle for 5 d. DES treatment resulted in a marked increase of serum prolactin (PRL), pituitary PRL content, PRL mRNA expression, pituitary weight, and pituitary proliferating cell nuclear antigen. DES treatment also increased pituitary VIP content and VIP mRNA levels, but not in the hypothalamus and cerebral cortex. Simultaneously, DES treatment decreased the pituitary TGF-β1 content and increased the pituitary content of vascular endothelial growth factor. VIP receptor antagonist partially reverted the effect of DES on serum PRL and pituitary PRL, proliferating cell nuclear antigen, TGF-β1, and vascular endothelial growth factor contents, as well as on pituitary weight, in a dose-dependent relation. These data suggest that pituitary VIP mediates the effect of E on lactotroph hyperplasia, pituitary TGF-β1, and angiogenesis.

Hypoxia-inducible Factor and Vascular Endothelial Growth Factor Are Expressed More Frequently in Embolized than in Nonembolized Cerebral Arteriovenous Malformations

Neurosurgery ◽  
2004 ◽  
Vol 55 (3) ◽  
pp. 663-670 ◽  
Author(s):  
Ulrich Sure ◽  
Elmar Battenberg ◽  
Astrid Dempfle ◽  
Wuttipong Tirakotai ◽  
Siegfried Bien ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Proliferating Cell Nuclear Antigen ◽  
Hypoxia Inducible Factor ◽  
Nuclear Antigen ◽  
Vascular Endothelial ◽  
Cerebral Arteriovenous Malformations ◽  
Hypoxia Inducible Factor 1Α ◽  
Endothelial Growth Factor ◽  
Proliferating Cell

Abstract OBJECTIVE: In previous studies, we documented a marked neoangiogenesis and endothelial proliferation in cerebral arteriovenous malformations (AVMs) that were embolized before surgery compared with those that were not embolized. We hypothesized that embolization caused a local hypoxia that promotes neoangiogenesis as a possible pathomechanism. To support this hypothesis, we now examined the angiogenesis-related proteins in a larger cohort of patients. In addition, we investigated hypoxia-inducible factor-1α as a possible protein operative during neoangiogenesis of cerebral AVMs. METHODS: Paraffin-embedded specimens of 56 AVMs obtained from surgical resection and 14 brain tissue controls were immunohistochemically stained with antibodies to proliferating cell nuclear antigen, MIB-1, vascular endothelial growth factor, Flk1, and hypoxia-inducible factor-1α by standard protocols. RESULTS: In AVMs treated with embolization before surgery (n = 35, 63%), the expression of hypoxia-inducible factor-1α (P = 0.0101) and vascular endothelial growth factor (P = 0.0007) was significantly higher (Fisher's exact test) than in patients who did not have previous endovascular treatment. Differences in the expression of Flk-1 (P = 0.0798) and proliferating cell nuclear antigen (P = 0.0423) were in the same direction but were not significant when corrected for multiple testing. CONCLUSION: Our results provide circumstantial evidence that a partial occlusion of cerebral AVMs might induce local hypoxia-related neoangiogenesis. To support these data, future animal studies should be performed.

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