Caenorhabditis Elegans and Angiogenesis

DergiPark: 541687tmsjAbstract: Angiogenesis is sprouting of new capillaries from already existing ones. It is a dynamic process that can be seen in every phase of human life. It is among the dynamic mechanisms of both physiological and pathological processes. Vascular endothelial growth factor is one of the many molecules that play a role in angiogenesis. Vascular endothelial growth factor is released specifically to the endothelium. It regulates mitogenesis, vascular tone, vascular permeability and vasodilatation in the vascular endothelium. Caenorhabditis elegans is a nematode used to detect and screen the developmental processes and genetic mutations. It is appropriate to study at the organism level to isolate cells and to demonstrate intercellular interactions in vivo. Polyvinyl fluoride-1 is a molecule that plays a role in the neural development of Caenorhabditis elegans. In addition, the polyvinyl fluoride-1 molecule is told to be effective in angiogenesis. Studies have shown that polyvinyl fluoride-1 binds to vascular endothelial growth factor receptor-1 and vascular endothelial growth factor receptor-2, but not to vascular endothelial growth factor receptor-3 and platelete derivated growth factor receptor ?. In the research of human umbilical vein endothelial lines, it was observed that polyvinyl fluoride-1 induced angiogenesis and vascular tube formation. These results suggest that Caenorhabditis elegans may have a very important role in vascular endothelial growth factor studies. Caenorhabditis elegans model is used in many scientific areas such as aging, nervous system and genetic changes. However, only a few laboratories around the world studied the Caenorhabditis elegans angiogenesis model. Besides, this model is not currently used in Turkey. This provides a great advantage in terms of the utilization of this model in angiogenesi

The Effects of Acyclovir on Angiogenesis in Chick Chorioallantoic Membrane Model

DergiPark: 1020964tmsjAims: This study aims to reveal the effects of acyclovir on angiogenesis and to assess the experimental doses. Methods: In the study, the chick chorioallantoic membrane model was used as an experimental model. Forty fertilized eggs were kept at 85-90% relative humidity, below 37°C until the fifth day post-fertil- ization, when the vessels in the chick chorioallantoic membrane model appeared and the drugs were applied. Four different concentrations of acyclovir were chosen to determine the mode of action and dose dependence: 3.55 mg/mL, 7.1 mg/mL, 14.2 mg/mL, and 28.4 mg/mL. Each of the 1 mL total acyclovir concentrations were applied to the chick chorioallantoic membrane surfaces. The chick chorioallantoic membranes treated with sterile distilled water were designated as controls. Eight eggs were used for each test group. After applying the drug, all the eggs were covered with transparent tape and kept under the same conditions throughout the experiment. The results were evaluated 48 hours after the drugs were administered and the results were recorded with a digital camera. Results: In our study, it was observed that 3.55 mg/mL acyclovir concentration shows the reduced density of capillaries around the pellet and no change in the number of capillaries. Both 7.1 mg/mL and 14.2 mg/mL concentrations of acyclovir caused a local reaction that was restricted to the membrane and it was attributed to local crystallization reaction. The concentration of 28.4 mg/mL had a toxic effect on the eggs. Conclusion: In this study, it was found that acyclovir has a very weak anti-angiogenic effect dose-dependently at the concentrations used. Considering that an observational model was used in our study, quantitative studies are needed for assessing anti-angiogenic effects in the future. There is also a need for further studies to elucidate the effects of acyclovir on vascular endothelial growth factor level and which stage of the angiogenesis-related process it is specifically effective on