Localization and Control of Expression of VEGF-A and the VEGFR-2 Receptor in Fetal Sheep Intestines

Holmes, Katrina; Charnock-Jones, D. Stephen; Forhead, Alison J.; Giussani, Dino A.; Fowden, Abigail L.; Licence, Diana; Kempster, Sarah; Smith, Gordon C. S.

doi:10.1203/pdr.0b013e31815f00e0

Cited by 21 publications

(15 citation statements)

References 16 publications

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“…Some stromal cells in the lamina propria of the villi also expressed VEGF. This localization pattern is consistent with previous studies [19,20]. An immunohistochemical study of normal foetal sheep intestine showed that VEGF was expressed in the muscularis and crypts, particularly prominent in the lamina propria and epithelial cells of the villi [20].…”

Section: Discussionsupporting

confidence: 92%

“…This localization pattern is consistent with previous studies [19,20]. An immunohistochemical study of normal foetal sheep intestine showed that VEGF was expressed in the muscularis and crypts, particularly prominent in the lamina propria and epithelial cells of the villi [20]. In another study using normal mouse intestine, VEGF was expressed mainly in epithelial cells of the crypts and became weaker through the tips of the villi [19].…”

Section: Discussionsupporting

confidence: 91%

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Intestinal and plasma VEGF levels in cirrhosis: the role of portal pressure

Huang

Haq

Utsumi

et al. 2012

J Cellular Molecular Medi

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Increased levels of intestinal VEGF are thought to worsen portal hypertension. The cause of the increase in the level of intestinal VEGF found during cirrhosis is not known. The aim of this study is to demonstrate a relationship between portal pressure (PP) and intestinal/ plasma VEGF levels in different stages of fibrosis/cirrhosis. In this experiment, rats were exposed to carbon tetrachloride (CCl4) for 6, 8 and 12 weeks. At the end of exposure, the three groups of rats exhibited three different stages of pathology: non-cirrhotic, early fibrotic and cirrhotic, respectively. For those rats and their age-matched controls, PP and intestinal/plasma VEGF levels were measured. Rats inhaling CCl4 for 12 weeks developed portal hypertension (18.02 ± 1.07 mmHg), while those exposed for 6 weeks (7.26 ± 0.58 mmHg) and for 8 weeks (8.55 ± 0.53 mmHg) did not. The rats exposed for 12 weeks also showed a 40% increase in the level of intestinal VEGF compared to the controls (P < 0.05), while those rats exposed to CCl4 inhalation for 6 and 8 weeks did not. There was a significant positive correlation between PP and intestinal VEGF levels (r2 = 0.4, P < 0.005). Plasma VEGF levels were significantly elevated in those rats exposed to 12 weeks of CCl4 inhalation (63.7 pg/ml, P < 0.01), compared to the controls (8.5 pg/ml). However, no correlation was observed between PP and plasma VEGF levels. It is concluded that portal pressure modulates intestinal VEGF levels during the development of cirrhosis.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 91%

Intestinal and plasma VEGF levels in cirrhosis: the role of portal pressure

Huang

Haq

Utsumi

et al. 2012

J Cellular Molecular Medi

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“…The few studies that have localized VEGF in intestinal tissues have reported inconsistent findings across studies and species [23–26]. Ubiquitous VEGF staining has been noted in fetal sheep small intestine [23] and in human adult tissues affected by inflammatory bowel disease [25, 26].…”

Section: Discussionmentioning

confidence: 99%

“…Ubiquitous VEGF staining has been noted in fetal sheep small intestine [23] and in human adult tissues affected by inflammatory bowel disease [25, 26]. Conversely, a study of human neonatal small intestine has reported VEGF expression solely in endothelial cells [24].…”

Section: Discussionmentioning

confidence: 99%

Intestinal Vascular Endothelial Growth Factor Is Decreased in Necrotizing Enterocolitis

Sabnis¹,

Carrasco²,

Liu³

et al. 2015

Neonatology

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Background: Decreased intestinal perfusion may contribute to the development of necrotizing enterocolitis (NEC). Vascular endothelial growth factor (VEGF) is an angiogenic protein necessary for the development and maintenance of capillary networks. Whether VEGF is dysregulated in NEC remains unknown. Objectives: The objective of this study was to determine whether intestinal VEGF expression is altered in a neonatal mouse model of NEC and in human NEC patients. Methods: We first assessed changes of intestinal VEGF mRNA and protein in a neonatal mouse NEC model before significant injury occurs. We then examined whether exposure to formula feeding, bacterial inoculation, cold stress and/or intermittent hypoxia affected intestinal VEGF expression. Last, we visualized VEGF protein in intestinal tissues of murine and human NEC and control cases by immunohistochemistry. Results: Intestinal VEGF protein and mRNA were significantly decreased in pups exposed to the NEC protocol compared to controls. Hypoxia, cold stress and commensal bacteria, when administered together, significantly downregulated intestinal VEGF expression, while they had no significant effect when given alone. VEGF was localized to a few single intestinal epithelial cells and some cells of the lamina propria and myenteric plexus. VEGF staining was decreased in murine and human NEC intestines when compared to control tissues. Conclusion: Intestinal VEGF protein is reduced in human and experimental NEC. Decreased VEGF production might contribute to NEC pathogenesis.

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“…As the fetal intestine prepares for birth and reliance upon enteral nutrition, development of its digestive and absorptive functions is stimulated by many factors, especially swallowing of amniotic fluid and fetal cortisol production (Sangild et al, 2000). Holmes et al (2008) recently demonstrated that vascularization of the intestine is also mediated by cortisol through its role in stimulating VEGF production. Although d 245 of gestation in cattle may be too early to observe VEGF upregulation caused by increased fetal cortisol, increased vascularity at d 245 in the current study suggests that the fetal intestine was undergoing increased angiogenesis as parturition neared.…”

Section: Fetal Effectsmentioning

confidence: 99%

Effects of stage of gestation and nutrient restriction during early to mid-gestation on maternal and fetal visceral organ mass and indices of jejunal growth and vascularity in beef cows1

Meyer

Reed

Vonnahme

et al. 2010

Journal of Animal Science

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The objectives were to evaluate effects of maternal nutrient restriction and stage of gestation on maternal and fetal visceral organ mass and indices of jejunal growth and vascularity in beef cows. Thirty multiparous beef cows (BW = 571 +/- 63 kg; BCS = 5.4 +/- 0.7) carrying female fetuses (d 30 of gestation) were allocated to receive a diet of native grass hay (CON; 12.1% CP, 70.7% IVDMD, DM basis) to meet NRC recommendations for BW gain during early gestation or a nutrient-restricted diet of millet straw (NR; 9.9% CP, 54.5% IVDMD, DM basis) to provide 68.1% of NE(m) and 86.7% of MP estimated requirements. On d 125 of gestation, 10 CON and 10 NR cows were killed and necropsied. Five remaining CON cows received the CON diet, and 5 NR cows were realimented with a concentrate supplement (13.2% CP, 77.6% IVDMD, DM basis) and the CON hay to achieve a BCS similar to CON cows by d 220 of gestation. Remaining cows were necropsied on d 245 of gestation. Cow BW and eviscerated BW (EBW) were less (P < 0.01) for NR than CON at d 125 but did not differ (P > 0.63) at d 245. Cows fed the CON diet had greater (P < 0.09) total gastrointestinal (GI) tract, omasal, and pancreatic weights. Stomach complex, ruminal, and liver weights were greater for CON than NR cows (P < 0.09) on d 125. Total GI, stomach complex, and pancreatic weights increased (P < 0.001) with day of gestation. Restricted cows had decreased (P = 0.09) duodenal RNA:DNA compared with CON. Duodenal DNA was less (P = 0.01) and jejunal RNA:DNA (P = 0.09) was greater for cows at d 125 vs. 245. Cow jejunal capillary area density increased with day of gestation (P = 0.02). Fetal BW and EBW were unaffected by dietary treatment (P > or = 0.32). Total GI tract and all components increased in mass with day of gestation (P < 0.001). Fetuses from NR dams had greater (P = 0.003) reticular mass at d 245 than CON fetuses. Fetuses from NR cows had greater (P = 0.02) percent jejunal proliferation at d 125 and greater (P = 0.03) total intestinal vascularity (mL) at d 245. Fetal jejunal DNA decreased (P = 0.09), RNA:DNA increased (P = 0.05), and total jejunal proliferating cells increased (P < 0.001) with day of gestation. Jejunal capillary area density, number density, and surface density were greater (P < 0.008) during late gestation. Results indicate that maternal and fetal intestines undergo changes during gestation, which can be affected by nutrient restriction and may partially explain differences observed in fetal development and postnatal performance.

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Localization and Control of Expression of VEGF-A and the VEGFR-2 Receptor in Fetal Sheep Intestines

Cited by 21 publications

References 16 publications

Intestinal and plasma VEGF levels in cirrhosis: the role of portal pressure

Intestinal and plasma VEGF levels in cirrhosis: the role of portal pressure

Intestinal Vascular Endothelial Growth Factor Is Decreased in Necrotizing Enterocolitis

Effects of stage of gestation and nutrient restriction during early to mid-gestation on maternal and fetal visceral organ mass and indices of jejunal growth and vascularity in beef cows1

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