Angiogenesis is repressed by ethanol exposure during chick embryonic development

Journal of Experimental Biology

Zhang

Wei

et al. 2015

Self Cite

In this study, we show that high-salt exposure dramatically increases chick mortality during embryo development. As embryonic mortality at early stages mainly results from defects in cardiovascular development, we focused on heart formation and angiogenesis. We found that high-salt exposure enhanced the risk of abnormal heart tube looping and blood congestion in the heart chamber. In the presence of high salt, both ventricular cell proliferation and apoptosis increased. The high osmolarity induced by high salt in the ventricular cardiomyocytes resulted in incomplete differentiation, which might be due to reduced expression of Nkx2.5 and GATA4. Blood vessel density and diameter were suppressed by exposure to high salt in both the yolk sac membrane (YSM) and chorioallantoic membrane models. In addition, high-salt-induced suppression of angiogenesis occurred even at the vasculogenesis stage, as blood island formation was also inhibited by high-salt exposure. At the same time, cell proliferation was repressed and cell apoptosis was enhanced by high-salt exposure in YSM tissue. Moreover, the reduction in expression of HIF2 and FGF2 genes might cause high-saltsuppressed angiogenesis. Interestingly, we show that high-salt exposure causes excess generation of reactive oxygen species (ROS) in the heart and YSM tissues, which could be partially rescued through the addition of antioxidants. In total, our study suggests that excess generation of ROS might play an important role in high-saltinduced defects in heart and angiogenesis.

Section: The Formation Of Blood Islands In the Extraembryonic Region mentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

The impact of high salt exposure on cardiovascular development in the early chick embryo

Journal of Experimental Biology

Zhang

Wei

et al. 2015

Self Cite

“…In our previously study, excess ethanol exposure was shown to inhibit embryonic angiogenesis through promoting superfluous ROS production during embryo development [40]. A.C. Tufan and N.L.…”

Section: Discussionmentioning

confidence: 99%

“…As reported in previous publications, ethanol exposure can induce excess ROS production [34,40]. 2,2-azobis (2-amidinopropane) dihydrochloride (AAPH, a free radicals generator 25, 40) was used to establish whether excess ROS could also induce vascular malformation and also in combination with vitamin C (an depressor of ROS production) to see whether the ethanol-or AAPH-induced inhibitive effect can be rescued (Figs.…”

Section: Ethanol Exposure Causes Excess Ros Generation During Blood Imentioning

confidence: 99%

Ethanol exposure leads to disorder of blood island formation in early chick embryo

Chen

Reproductive Toxicology

et al. 2017

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exposure leads to disorder of blood island formation in early chick embryo.Reproductive Toxicology http://dx.doi.org/10. 1016/j.reprotox.2017.08.003 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. 2,2′-azobis-amidinopropane dihydrochloride, a ROS inducer, which gave a similar anti-vasculogenesis effect as ethanol and this anti-vasculogenesis effect could be reversed by vitamin C. Overall, exposing early chick embryos to ethanol represses blood island progenitor cell migration but disturbed differentiation at a different stage, so that the disorder of blood island formation occurs through excess ROS production and altered vascular-associated gene expression.

Int J Pharm Sci Dev Res

“…The morphology of the CAMs was photographed. The areas occupied by the blood vessel were measured by Intel Integrated Performance Primitives (IPP) [14]. The blood vessel density was the percentage of area occupied by the blood vessels over the whole area under the picture's field [15].…”

mentioning

confidence: 99%

Edaravone Protects against Vascular Oxidative Damage Induced by AAPH in Chick Embryo

Wan¹,

Luo²,

Jie³

et al. 2016

Background: Edaravone (Eda) is a free-radical scavenger which is used in treating stroke, cerebral hemorrhage and some other diseases in clinic. However, it's antioxygenation during development is still unknown.Method: An oxidative damage model was established in chick embryo by using a generator of free radicals, 2,2'-azobis[2-methylpropionamidine] dihydrochloride (AAPH). The mortality rate and embryo's weight were measured to detect whether retarded growth happened. In order to observe the blood vessels, the yolk-sac blood vessels and CAM blood vessels density were observed. The malondialdehyde (MDA) content and superoxide dismutase (SOD) enzymatic activity were detected to evaluate the oxidative damage in the chick embryo.Result: In this model, embryo development and angiogenesis were heavily affected by AAPH. However, Eda alleviated the growth retardation and anti-angiogenesis induced by AAPH. After AAPH treatment, the MDA content increased and SOD enzymatic activity declined which was also mitigated by Eda. Conclusion:Overall, our research revealed that Eda mitigated embryonic anti-angiogenesis induced by oxidative damage after AAPH treatment, which may be helpful for future clinical studies.stress [7]. During the pregnancy period, pregnant women suffer from emotional fluctuation, environmental pollution, life pressure, improper diet and so on. Women are exposed to oxidative stress and the fetuses are easily affected.In this research, the chick embryo was chosen as the experimental animal, as chick embryo is suitable for evaluating angiogenesis. The chick embryo holds a wide range of advantages, with low cost and less ethical arguments [8]. It is a classical development model where the chick yolk sac and chorioallantoic membranes (CAMs) are extensively used in research related to angiogenesis. Besides, the growth cycle of chick embryo is short, where 21 days for chick embryo is similar to 10 months for human [9]. Moreover, it is a simple spinal biological, whose growth process can be easily observed [10].In order to mimic chronic oxidative stress exposed to human, 2,2'-azobis[2-methylpropionamidine] dihydrochloride (AAPH) was repeatedly treated in a small dose. AAPH is an azo compound and completely dissolved in alkyl, peroxyl and alkoxyl radicals at physiological temperature [11]. AAPH has been widely used to study the mechanism of oxidative stress [12,13]. In our previous experiments, the chick embryo on embryo development day (EDD) 9 was treated with a large dose of AAPH. After incubation for 24 hours, the chick embryo suffered from oxidative stress and the cardiovascular system was affected [7]. Nevertheless, whether chronic oxidative stress affects the development of embryos is still unclear. In our study, AAPH was injected to chick embryos in long-term and the development of chick embryo was observed. AbbreviationsEda: Edaravone; 3-methyl-1-phenyl-2-pyrazolin-5-one; AAPH: 2,2'-azobis [2-methylpropionamidine] IntroductionEdaravone (3-methyl-1-phenyl-2-pyrazolin-5-one, Eda), a free-radical sc...