scholarly journals The effect of methenamine on vascular development: Experimental investigation using in vivo and insilico methods

Author(s):  
Hadi Tavakkoli ◽  
Masoud Imani ◽  
Seyyed Mohammad Rahchamani ◽  
Mohsen Rezvani

Background: Methenamine is a worldwide antibacterial agent for urinary system infections in human and animals. The effect of methenamine consumption during early phase of pregnancy is not fully clarified in previous studies. Vascular development is the essential part of the early embryonic growth. Objective: In this study, we used chicken chorioallantoic membrane to evaluate the effects of methenamine administration on angiogenesis process as a model. Materials and Methods: In this experimental study, 20 Ross 308 eggs (mean weight 55 ± 4) were incubated. The eggs were divided into two equal groups (n = 10/each). In the first group, methenamine (150 mg/kg egg weight) was injected on the shell membrane, and in the second group (control group) phosphate-buffered saline as injected. Methenamine was inoculated at 96 and 120 hr after incubation; 24 hr after the last inoculation, the eggs were removed and the egg’s shell was incised. Then, the development of vascular network and vascular endothelial growth factor A expression was evaluated. Results: Angiogenesis was significantly decreased after methenamine treatment. The indexes such as areas containing vessels, the vessels’ length, the percentage of angiogenesis developing areas, and vascular complexity in the treatment group receiving methenamine were significantly reduced compared to the control group. Vascular endothelial growth factor A expression was suppressed in the methenamine treated group. Conclusion: According to the achieved results, it was defined that methenamine could have an inhibitory effect on the growth and development procedures of extraembryonic vasculature. Key words: Methenamine, Angiogenesis modulating agents, Vascular endothelial growth factor A, Extraembryonic membranes.

2004 ◽  
Vol 89 (3) ◽  
pp. 1415-1422 ◽  
Author(s):  
Olin D. Liang ◽  
Thomas Korff ◽  
Jessica Eckhardt ◽  
Jasmin Rifaat ◽  
Nelli Baal ◽  
...  

Abstract The molecular coordination between angiogenesis and vascular remodeling is a critical step for the development of a functional vasculature in the placenta and the uterus during pregnancy. The oncodevelopmental albumin homolog α-fetoprotein (AFP) is mainly synthesized in the developing fetus, and its expression has been found to be associated with highly vascularized tumors in the adult. In this study, we investigated the angiogenic activity of AFP and its possible role in the fetomaternal unit. Immunohistochemical studies revealed that the AFP-binding protein(s) is expressed in blood vessels of chorionic villi from placentae of the second and the third but not of the first trimester during pregnancy. At low concentrations, AFP directly stimulates or enhances, respectively, vascular endothelial growth factor-induced proliferation and sprout formation of endothelial cells isolated from the placenta and the uterus possibly by a MAPK-dependent pathway. Furthermore, AFP enhances blood vessel formation in a chick chorioallantoic membrane assay in vivo. Interestingly, AFP has no proliferative or migratory effects on endothelial cells isolated from the umbilical vein in the absence of vascular endothelial growth factor. These data indicate that AFP may act as a specific proangiogenic factor of endothelial cells within the fetomaternal unit during advanced stages in pregnancy.


2015 ◽  
Vol 227 (2) ◽  
pp. R31-R50 ◽  
Author(s):  
Kevin M Sargent ◽  
Renee M McFee ◽  
Renata Spuri Gomes ◽  
Andrea S Cupp

Testis development from an indifferent gonad is a critical step in embryogenesis. A hallmark of testis differentiation is sex-specific vascularization that occurs as endothelial cells migrate from the adjacent mesonephros into the testis to surround Sertoli-germ cell aggregates and induce seminiferous cord formation. Manyin vitroexperiments have demonstrated that vascular endothelial growth factor A (VEGFA) is a critical regulator of this process. Both inhibitors to VEGFA signal transduction and excess VEGFA isoforms in testis organ cultures impaired vascular development and seminiferous cord formation. However,in vivomodels using mice which selectively eliminated all VEGFA isoforms: in Sertoli and germ cells (pDmrt1-Cre;Vegfa−/−); Sertoli and Leydig cells (Amhr2-Cre;Vegfa−/−) or Sertoli cells (Amh-Cre;Vegfa−/−andSry-Cre;Vegfa−/−) displayed testes with observably normal cords and vasculature at postnatal day 0 and onwards. Embryonic testis development may be delayed in these mice; however, the postnatal data indicate that VEGFA isoforms secreted from Sertoli, Leydig or germ cells are not required for testis morphogenesis within the mouse. AVegfasignal transduction array was employed on postnatal testes fromSry-Cre;Vegfa−/−versus controls.Ptgs1(Cox1) was the only upregulated gene (fivefold). COX1 stimulates angiogenesis and upregulates, VEGFA, Prostaglandin E2 (PGE2) and PGD2. Thus, other gene pathways may compensate for VEGFA loss, similar to multiple independent mechanisms to maintain SOX9 expression. Multiple independent mechanism that induce vascular development in the testis may contribute to and safeguard the sex-specific vasculature development responsible for inducing seminiferous cord formation, thus ensuring appropriate testis morphogenesis in the male.


2021 ◽  
Vol 31 (Supplement_2) ◽  
Author(s):  
Armando Caseiro ◽  
Carla Ferreira ◽  
Ana Margarida Silva ◽  
João Paulo Figueiredo ◽  
Telmo Pereira

Abstract Background Resveratrol (3,4',5-trihydroxystilbene) (RSV) is one of the main non-flavonoid natural polyphenol compounds. Evidence suggests that RSV has a key role in preventing a variety of pathological processes because of its benefits, including anti-aging, anti-inflammatory, and cardiovascular disease prevention. Vascular endothelial growth factor (VEGF) is responsible for vasculogenesis and angiogenesis, and its expression is influenced by RSV. Vascular nitric oxide (NO) acts to relax smooth muscle cells by preventing thrombogenic processes. It has been shown in vitro and in vivo that RSV is involved in NO metabolism. The aim of this work was evaluate the effects of regular low-dose RSV consumption by determining serum VEGF and NO levels compared to a control group. Methods The study involved 27 clinically healthy individuals, divided into a control group (placebo) and an intervention group, supplemented with 100mg RSV/day. The VEGF levels were determined by slot blot technique and NO levels were determined by spectrophotometry before (T0) and after 30 days (T1) of supplementation. Results The VEGF and NO levels slightly decrease from T0 to T1 moment in both study groups, showing a higher decrease in both parameters in the control group compared to the intervention group, but the variation was not statistically significant. Conclusions Daily supplementation with RSV is associated with benefits at the VEGF level as well as at the vascular level. However, further studies with a larger number of participants are needed to confirm the effects of RSV on VEGF and NO levels.


Author(s):  
Christiane Claaßen ◽  
Miriam Dannecker ◽  
Jana Grübel ◽  
Maria-Elli Kotzampasi ◽  
Günter E. M. Tovar ◽  
...  

AbstractBio-based coatings and release systems for pro-angiogenic growth factors are of interest to overcome insufficient vascularization and bio-integration of implants. This study compares different biopolymer-based coatings on polyethylene terephthalate (PET) membranes in terms of coating homogeneity and stability, coating thickness in the swollen state, endothelial cell adhesion, vascular endothelial growth factor (VEGF) release and pro-angiogenic properties. Coatings consisted of carbodiimide cross-linked gelatin type A (GelA), type B (GelB) or albumin (Alb), and heparin (Hep), or they consisted of radically cross-linked gelatin methacryloyl-acetyl (GM5A5) and heparin methacrylate (HepM5). We prepared films with thicknesses of 8–10 µm and found that all coatings were homogeneous after washing. All gelatin-based coatings enhanced the adhesion of primary human endothelial cells compared to the uncoated membrane. The VEGF release was tunable with the loading concentration and dependent on the isoelectric points and hydrophilicities of the biopolymers used for coating: GelA-Hep showed the highest releases, while releases were indistinguishable for GelB-Hep and Alb-Hep, and lowest for GM5A5-HepM5. Interestingly, not only the amount of VEGF released from the coatings determined whether angiogenesis was induced, but a combination of VEGF release, metabolic activity and adhesion of endothelial cells. VEGF releasing GelA-Hep and GelB-Hep coatings induced angiogenesis in a chorioallantoic membrane assay, so that these coatings should be considered for further in vivo testing.


Author(s):  
YanuarEka P. ◽  
Hendy Hendarto ◽  
Widjiati .

Retrograde menstruation lead to I Kappa B Kinase (IKK) fosforilation in peritoneum macrophage and cause secretion of proinflammatory cytokine interleukin1β then stimulate endometriosis cell to produce Vascular Endothelial Growth Factor which lead to increasing of endometriosis lession seen as endometriosis implant area. Cytokine secretion was inhibited through prevention of NF-κB activation by dragon red fruit rind extract (Hylocereuspolyrhizus). The aim of this reserach is to know the effect of dragon red fuit rind extract with 0,25; 0,5; and 1 mg/g bodyweight dosage toward IL-1β, VEGF expression and implant area in endometriosis mice model. The design of this experiment was randomized post test only control group design.Endometrios mice model were made in 14 days and split into two group, positive control group and treatment group after two week negative control group and postive control group were given Na-CMC 0,5% solution consequetively, and treatment group were given dragon red fruit extract with different dosage. Signification number for IL-1β is p>0,05, signification number for VEGF is p>0,05, and implant area signification number is p>0,05. Administration of dragon red fruit rind extract can decrease IL-1β, VEGF, and implant area.


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