­Changes in the osmolarity of the embryonic microenvironment induce neural tube defects

Jin, Yimei; Wang, Guang; Zhang, Nuan; Wei, Yifan; Li, Shuai; Chen, You‐Peng; Chuai, Manli; Lee, Henry Siu Sum; Hocher, Berthold; Yang, Xuesong

doi:10.1002/mrd.22482

Cited by 8 publications

(10 citation statements)

References 25 publications

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“…However, we found the neural tube of this level re-open in the experimental groups on the 4.5 day. This phenotype is similar with the high-salt treated chick embryos in our previously study (Jin et al, 2015). Thus, we speculated that the opening of the neural tubes was related to the abnormal cell proliferation and apoptosis, so that we performed PCNA and Tunel staining.…”

Section: Discussionsupporting

confidence: 83%

From the Cover: Exposing Imidacloprid Interferes With Neurogenesis Through Impacting on Chick Neural Tube Cell Survival

Li¹,

Wang²,

Zhang³

et al. 2016

Toxicol. Sci.

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As a neonicotinoid pesticide, imidacloprid is widely used to control insects in agriculture and fleas on domestic animals. However, it is not known whether imidacloprid exposure negatively affects neurogenesis during embryonic development. In this study, using a chick embryo model, we investigated the effects of imidacloprid exposure on neurogenesis at the earliest stage and during late-stage embryo development. Exposing HH0 chick embryos to imidacloprid in EC culture caused neural tube defects (NTDs) and neuronal differentiation dysplasia as determined by NF/Tuj1 labeling. Furthermore, we found that F-actin accumulation on the apical side of the neural tube was suppressed by exposure to imidacloprid, and the expression of BMP4 and Shh on the dorsal and ventral sides of the neural tubes, respectively, were also reduced, which in turn affects the dorsolateral hinge points during bending of the neural plate. In addition, exposure to imidacloprid reduced cell proliferation and increased cell apoptosis, as determined by pHIS3 labeling and TUNEL staining, respectively, also contributing to the malformation. We obtained similar results in late-stage embryos exposed to imidacloprid. Finally, a bioinformatics analysis was employed to determine which genes identified in this study were involved in NTDs. The experimental evidence and bioinformatics analysis suggested that imidacloprid exposure during chick embryo development could increase the risk of NTDs and neural dysplasia.

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Section: Discussionsupporting

confidence: 83%

From the Cover: Exposing Imidacloprid Interferes With Neurogenesis Through Impacting on Chick Neural Tube Cell Survival

Li¹,

Wang²,

Zhang³

et al. 2016

Toxicol. Sci.

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“…This represents one kind of strength and a weakness of the model. In our previous study, we demonstrated that chick embryos exposed to excess salt have impaired retina and lens development (Chen et al, 2014) and induced neural tube defects (Jin et al, 2015). Here, we investigate the adverse impact of high-salt-induced hyperosmolarity on cardiovascular development using early chick embryos.…”

Section: Introductionmentioning

confidence: 94%

“…The eggs were incubated in a humidified incubator (Yiheng Instrument, Shanghai, China) at 38°C and 70% humidity. After 36 h of incubation, the chick embryos were treated as previously described (Chen et al, 2014;Jin et al, 2015): in brief, 2 ml albumen was removed from an egg and the egg was then injected with 500 µl of three different concentrations of NaCl. For the control group, we injected 0.7% NaCl (calculated final osmolality of the egg was 240 mosm l −1 ); for the 300 mosm l −1 group, we injected 16.85% NaCl (calculated final osmolality of the egg, 300 mosm l −1 ); for the vitamin C (VC) rescue experiment , we administered VC (0.5 mg egg −1 ) after injection of 16.85% NaCl.…”

Section: Chick Embryosmentioning

confidence: 99%

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

Wang

Zhang

Wei

et al. 2015

Journal of Experimental Biology

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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.

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“…Bone morphogenetic protein (BMP) signaling and Sonic hedgehog (Shh) signaling jointly regulate the formation of DHLP, subsequently affecting the closure neural tube [42]. Neural tube development is highly dependent on the precisely spatiotemporal regulation of bone morphogenetic protein 4 (BMP4), paired box 7 (Pax7) and Sonic hedgehog (Shh) genes in the dorsal side of the tube [43]. After exposure to OA, the inhibition of BMP4and Shh expression in the dorsal neural tube suggests that OA exposure could also affect the formation of DHLP, and then disturb the subsequent folding process, and ultimately lead to the incomplete closure of the neural tube.…”

Section: Discussionmentioning

confidence: 99%

Okadaic Acid Exposure Induced Neural Tube Defects in Chicken (Gallus gallus) Embryos

Jiao

Wang

et al. 2021

Marine Drugs

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Okadaic acid (OA) is an important liposoluble shellfish toxin distributed worldwide, and is mainly responsible for diarrheic shellfish poisoning in human beings. It has a variety of toxicities, including cytotoxicity, embryonic toxicity, neurotoxicity, and even genotoxicity. However, there is no direct evidence of its developmental toxicity in human offspring. In this study, using the chicken (Gallus gallus) embryo as the animal model, we investigated the effects of OA exposure on neurogenesis and the incidence of neural tube defects (NTDs). We found that OA exposure could cause NTDs and inhibit the neuronal differentiation. Immunofluorescent staining of pHI3 and c-Caspase3 demonstrated that OA exposure could promote cell proliferation and inhibit cell apoptosis on the developing neural tube. Besides, the down-regulation of Nrf2 and increase in reactive oxygen species (ROS) content and superoxide dismutase (SOD) activity in the OA-exposed chicken embryos indicated that OA could result in oxidative stress in early chick embryos, which might enhance the risk of the subsequent NTDs. The inhibition of bone morphogenetic protein 4 (BMP4) and Sonic hedgehog (Shh) expression in the dorsal neural tube suggested that OA could also affect the formation of dorsolateral hinge points, which might ultimately hinder the closure of the neural tube. Transcriptome and qPCR analysis showed the expression of lipopolysaccharide-binding protein (LBP), transcription factor AP-1 (JUN), proto-oncogene protein c-fos (FOS), and C-C motif chemokine 4 (CCL4) in the Toll-like receptor signaling pathway was significantly increased in the OA-exposed embryos, suggesting that the NTDs induced by OA might be associated with the Toll-like receptor signaling pathway. Taken together, our findings could advance the understanding of the embryo–fetal developmental toxicity of OA on human gestation.

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Changes in the osmolarity of the embryonic microenvironment induce neural tube defects

Cited by 8 publications

References 25 publications

From the Cover: Exposing Imidacloprid Interferes With Neurogenesis Through Impacting on Chick Neural Tube Cell Survival

From the Cover: Exposing Imidacloprid Interferes With Neurogenesis Through Impacting on Chick Neural Tube Cell Survival

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

Okadaic Acid Exposure Induced Neural Tube Defects in Chicken (Gallus gallus) Embryos

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­Changes in the osmolarity of the embryonic microenvironment induce neural tube defects

Cited by 8 publications

References 25 publications

From the Cover: Exposing Imidacloprid Interferes With Neurogenesis Through Impacting on Chick Neural Tube Cell Survival

From the Cover: Exposing Imidacloprid Interferes With Neurogenesis Through Impacting on Chick Neural Tube Cell Survival

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

Okadaic Acid Exposure Induced Neural Tube Defects in Chicken (Gallus gallus) Embryos

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Product

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Changes in the osmolarity of the embryonic microenvironment induce neural tube defects