scholarly journals N-carbamylglutamate and L-arginine improved maternal and placental development in underfed ewes

Reproduction ◽  
2016 ◽  
Vol 151 (6) ◽  
pp. 623-635 ◽  
Author(s):  
Hao Zhang ◽  
Lingwei Sun ◽  
Ziyu Wang ◽  
Mingtian Deng ◽  
Haitao Nie ◽  
...  
Keyword(s):  
Growth Factor ◽  
Dietary Supplementation ◽  
Late Gestation ◽  
Vascular Endothelial ◽  
Placental Development ◽  
Fetal Plasma ◽  
Total Antioxidant ◽  
Endocrine Status ◽  
Endothelial Growth Factor ◽  
Hu Sheep

AbstractThe objectives of this study were to determine how dietary supplementation ofN-carbamylglutamate (NCG) and rumen-protected L-arginine (RP-Arg) in nutrient-restricted pregnant Hu sheep would affect (1) maternal endocrine status; (2) maternal, fetal, and placental antioxidation capability; and (3) placental development. From day 35 to day 110 of gestation, 32 Hu ewes carrying twin fetuses were allocated randomly into four groups: 100% of NRC-recommended nutrient requirements, 50% of NRC recommendations, 50% of NRC recommendations supplemented with 20g/day RP-Arg, and 50% of NRC recommendations supplemented with 5g/day NCG product. The results showed that in maternal and fetal plasma and placentomes, the activities of total antioxidant capacity and superoxide dismutase were increased (P<0.05); however, the activity of glutathione peroxidase and the concentration of maleic dialdehyde were decreased (P<0.05) in both NCG- and RP-Arg-treated underfed ewes. The mRNA expression of vascular endothelial growth factor and Fms-like tyrosine kinase 1 was increased (P<0.05) in 50% NRC ewes than in 100% NRC ewes, and had no effect (P>0.05) in both NCG- and RP-Arg-treated underfed ewes. A supplement of RP-Arg and NCG reduced (P<0.05) the concentrations of progesterone, cortisol, and estradiol-17β; had no effect on T4/T3; and improved (P<0.05) the concentrations of leptin, insulin-like growth factor 1, tri-iodothyronine (T3), and thyroxine (T4) in serum from underfed ewes. These results indicate that dietary supplementation of NCG and RP-Arg in underfed ewes could influence maternal endocrine status, improve the maternal–fetal–placental antioxidation capability, and promote fetal and placental development during early-to-late gestation.

Plasma Total Antioxidant Activity in Comparison with Plasma NO and VEGF Levels in Patients with Metabolic Syndrome

Angiology ◽  
2008 ◽  
Vol 60 (1) ◽  
pp. 87-92 ◽  
Author(s):  
Marcin Barylski ◽  
Edward Kowalczyk ◽  
Maciej Banach ◽  
Julita Ciećwierz ◽  
Lucjan Pawlicki ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Metabolic Syndrome ◽  
Vascular Endothelial Growth Factor ◽  
Antioxidant Activity ◽  
Growth Factor ◽  
Vascular Endothelial ◽  
Total Antioxidant Activity ◽  
Total Antioxidant ◽  
Endothelial Growth Factor ◽  
Healthy Participants

Introduction The aim of our study was to estimate plasma antioxidant activity as well as plasma nitric oxide (NO) and vascular endothelial growth factor levels in patients with metabolic syndrome compared with healthy participants. Material and Methods Fifty patients (24 women and 26 men, mean age 55.9 ± 11.8 years) with metabolic syndrome were compared with 25 healthy participants (12 women and 13 men, mean age 54.2 ± 12.8 years). Plasma total antioxidant activity and plasma levels of NO and VEGF were determined in all participants. Results In the patients with metabolic syndrome, plasma total antioxidant activity, nitric oxide, and vascular endothelial growth factor were significantly lower ( P < .001) than that observed in healthy participants (3.2 ± 1.6 vs 6.4 ± 2.1 mM/L), (6.3 ± 2.2 vs 9.8 ± 2.7 μM/L), and 71.0 ± 16.9 vs 137.5 ± 12.6 pg/mL), respectively. Conclusions Decreased plasma total antioxidant activity, NO, and VEGF levels in patients with metabolic syndrome reflect significant endothelial dysfunction. This suggests that oxidation–reduction balance disorders might play an important role in this process

scholarly journals Comparison of expression patterns for placenta growth factor, vascular endothelial growth factor (VEGF), VEGF-B and VEGF-C in the human placenta throughout gestation

1998 ◽  
Vol 159 (3) ◽  
pp. 459-467 ◽  
Author(s):  
DE Clark ◽  
SK Smith ◽  
D Licence ◽  
AL Evans ◽  
DS Charnock-Jones
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Expression Patterns ◽  
In Situ Hybridisation ◽  
Extravillous Trophoblast ◽  
Vascular Endothelial ◽  
Placenta Growth Factor ◽  
Placental Development ◽  
New Members ◽  
Endothelial Growth Factor

Angiogenesis and vascular transformation are important processes in the normal development of the placenta. Vascular endothelial growth factor (VEGF) is a potent angiogenic growth factor and is thought to be important for placental development. Recently several new members of this family have been described. In this study we used in situ hybridisation to localise which cells in the placenta expressed mRNA for VEGF, placenta growth factor (PlGF), VEGF-B and VEGF-C. We were unable to find any message for either VEGF-B or VEGF-C in the placenta, suggesting that only low levels are produced which this method was unable to detect. The mRNA encoding VEGF was found to be produced by cells within the villous mesenchyme, decidual macrophages and decidual glands but, in contrast to our previous findings, not by trophoblast. The mRNA encoding PlGF was produced in large amounts by villous cytotrophoblast, syncytiotrophoblast and extravillous trophoblast. The mRNAs encoding VEGF and PlGF were thus not co-localised and it appears that there is unlikely to be any significant production of VEGF/PlGF heterodimer in the placenta.

scholarly journals Dietary l-arginine supplementation enhances intestinal development and expression of vascular endothelial growth factor in weanling piglets

2011 ◽  
Vol 105 (5) ◽  
pp. 703-709 ◽  
Author(s):  
Kang Yao ◽  
Shu Guan ◽  
Tiejun Li ◽  
Ruilin Huang ◽  
Guoyao Wu ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Plasma Concentrations ◽  
Dietary Supplementation ◽  
Control Group ◽  
Vascular Endothelial ◽  
Intestinal Development ◽  
Soyabean Meal ◽  
Endothelial Growth Factor ◽  
Arginine Supplementation

Oral administration of l-arginine has been reported to prevent gut disease in human infants. However, little is known about the effects of dietary arginine supplementation on intestinal development of weaned piglets. In the present study, twenty 21-d-old castrated piglets with 5·3 (sem 0·13) kg body weight (BW) were weaned from sows, individually housed and randomly assigned to one of the two maize- and soyabean meal-based diets supplemented with 0 or 1 % l-arginine. After consuming the diets for 7 d, six pigs were randomly selected from each group to obtain various tissues. Compared with control pigs, dietary supplementation with 1 % l-arginine did not affect feed intake but enhanced (P < 0·05) the relative weight of the small intestine (+33 %), daily BW gain (+38 %) and feed efficiency (+28 %). The villus height of the duodenum, jejunum and ileum in arginine-supplemented piglets was 21, 28 and 25 % greater (P < 0·05) than in the non-supplemented control group. Arginine supplementation increased (P < 0·05) protein levels for vascular endothelial growth factor (VEGF) in duodenal, jejunal and ileal mucosae by 14, 39 and 35 %, respectively. Compared with the control group, dietary supplementation with 1 % l-arginine increased (P < 0·05) plasma concentrations of arginine and insulin (+36 %), and decreased (P < 0·05) plasma concentrations of cortisol ( − 33 %), NH3 ( − 21 %) and urea ( − 19 %). These results indicate that arginine supplementation enhances intestinal growth, development and expression of VEGF in early-weaned pigs fed a maize- and soyabean meal-based diet. The findings may have important implications for neonatal pigs under stressful or diseased conditions.

63 Inhibition of CXCR4 at the fetal-maternal interface during placentation results in altered production of vascular endothelial growth factor receptors in the placenta on Day 90 of pregnancy

2020 ◽  
Vol 32 (2) ◽  
pp. 157
Author(s):  
J. M. Ervin ◽  
S. Z. McIntosh ◽  
C. L. Runyan ◽  
R. L. Ashley
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Animal Model ◽  
Growth Factor ◽  
Day Treatment ◽  
Vegf Receptor ◽  
Vascular Endothelial ◽  
Placental Development ◽  
Fetal Survival ◽  
Pregnant Sheep ◽  
Endothelial Growth Factor

Placental development is characterised by extensive angiogenesis and vascularization; if these processes are compromised, placental dysfunction occurs, which is the underlying cause of complications such as preeclampsia and intrauterine growth restriction. The signalling axis initiated by chemokine ligand 12 (CXCL12) and its receptor CXCR4 stimulate angiogenesis critical to placental vascularization. Our laboratory and others demonstrated stimulation of vascular endothelial growth factor (VEGF) synthesis by CXCL12/CXCR4 signalling, and recently, we reported less production of the VEGF receptor, FLT-1, on Day 20 in pregnant sheep following interference of intrauterine CXCL12-dependent signalling. While no animal model fully recapitulates human placentation, the sheep is arguably the most applicable animal model to study fetal-maternal interactions and placentation. Based on our studies, we hypothesised that inhibiting CXCR4 at the fetal-maternal interface during initial placentation alters placental production of VEGF receptors, FLT-1 and KDR, at mid-gestation. To test this hypothesis, AMD3100, a CXCR4 antagonist, was used to elucidate the role of CXCL12/CXCR4 signalling at the ovine fetal-maternal interface. On Day 12 post-breeding, osmotic pumps were surgically installed and delivered either AMD3100 or phosphate-buffered saline (PBS) into the uterine lumen ipsilateral to the corpus luteum for either 7 days (n=7 PBS and n=8 AMD3100) or 14 days (n=7 PBS and n=8 AMD3100). The objectives were to determine whether disruption of the CXCL12/CXCR4 axis during placentation affects fetal survival and alters VEGF receptor synthesis and whether duration of CXCR4 inhibition affects placental vascular remodelling. On Day 90 of pregnancy, ewes were anaesthetised; reproductive tracts were removed; and maternal caruncle (CAR) and fetal cotyledon (COT) components were separated, snap frozen in liquid nitrogen, and stored at −80°C until protein isolation. Pregnancy success was not affected by treatment or duration of treatment (71% PBS vs. 62% AMD3100 for 7 days; 85% PBS vs. 62% AMD3100 for 14 days). In addition, fetal weight on Day 90 (530.8±28.2 g PBS vs. 540.5±20.3g AMD3100 for 7 days; 494.3±23.9g PBS vs. 532.7±11.8g AMD3100 for 14 days) was not affected by treatment. Immunoblotting was used to detect protein abundance, and an unpaired two-tailed Student's t-test was used to determine significant changes. Greater FLT-1 (P&lt;0.05) was evident in CAR and COT tissue on Day 90 for both the 7-day treatment (0.92±0.16 CAR PBS vs. 1.48±0.18 CAR AMD3100; 0.12±0.16 COT PBS vs. 0.62±0.16 COT AMD3100) and the 14-day treatment (0.18±0.05 CAR PBS vs. 0.43±0.001 CAR AMD3100; 0.04±0.005 COT PBS vs. 0.11±0.02 COT AMD3100) of CXCR4 inhibition compared with controls, whereas KDR levels did not change (P&gt;0.05). Interestingly, elevated FLT-1, but not KDR, is a marker of preeclampsia in women, and because of its role as a VEGF scavenger, overexpression of FLT-1 often leads to an anti-angiogenic state. We suggest that CXCL12/CXCR4 signalling during initial placental development serves as an upstream regulator of placental vascularization, thereby ensuring appropriate placental development.

scholarly journals Deletion of Vascular Endothelial Growth Factor C (VEGF-C) and VEGF-D Is Not Equivalent to VEGF Receptor 3 Deletion in Mouse Embryos

2008 ◽  
Vol 28 (15) ◽  
pp. 4843-4850 ◽  
Author(s):  
Paula Haiko ◽  
Taija Makinen ◽  
Salla Keskitalo ◽  
Jussi Taipale ◽  
Marika J. Karkkainen ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Early Embryo ◽  
Vegf Receptor ◽  
Tissue Fluid ◽  
Vascular Endothelial ◽  
Placental Development ◽  
Independent Functions ◽  
Factor C ◽  
Endothelial Growth Factor

ABSTRACT Lymphatic vessels play an important role in the regulation of tissue fluid balance, immune responses, and fat adsorption and are involved in diseases including lymphedema and tumor metastasis. Vascular endothelial growth factor (VEGF) receptor 3 (VEGFR-3) is necessary for development of the blood vasculature during early embryogenesis, but later, VEGFR-3 expression becomes restricted to the lymphatic vasculature. We analyzed mice deficient in both of the known VEGFR-3 ligands, VEGF-C and VEGF-D. Unlike the Vegfr3 −/− embryos, the Vegfc −/−; Vegfd −/− embryos displayed normal blood vasculature after embryonic day 9.5. Deletion of Vegfr3 in the epiblast, using keratin 19 (K19) Cre, resulted in a phenotype identical to that of the Vegfr3 −/− embryos, suggesting that this phenotype is due to defects in the embryo proper and not in placental development. Interestingly, the Vegfr3 neo hypomorphic mutant mice carrying the neomycin cassette between exons 1 and 2 showed defective lymphatic development. Overexpression of human or mouse VEGF-D in the skin, under the K14 promoter, rescued the lymphatic hypoplasia of the Vegfc +/− mice in the K14-VEGF-D; Vegfc +/− compound mice, suggesting that VEGF-D is functionally redundant with VEGF-C in the stimulation of developmental lymphangiogenesis. Our results suggest VEGF-C- and VEGF-D-independent functions for VEGFR-3 in the early embryo.

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