Embryogenesis of triple neural tube defects: sonic hedgehog—a key?

Mahalik, Santosh Kumar; Vaze, Dhananjay; Lyngdoh, Toijam Soni; Tewari, Manoj Kumar; Narasimhan, Kannan Laksmi

doi:10.1016/j.jpedsurg.2010.09.103

Cited by 5 publications

(4 citation statements)

References 11 publications

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“…The formation of dorsolateral hinge points (DHLPs) plays an important role in neural tube closure during neurogenesis [41]. 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].…”

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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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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“…The formation of dorsolateral hinge points (DHLP) plays an important role in neural tube closure during neurogenesis [48]. Bone morphogenetic protein (BMP) signaling and Sonic hedgehog (Shh) signaling jointly regulate the formation of DHLP, subsequently affecting the closure neural tube [49]. 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 [50].…”

Section: Discussionmentioning

confidence: 99%

Okadaic acid exposure induced neural tube defects in chicken (Gallus gallus) embryos

Jiao¹,

Wang²,

Li³

et al. 2020

Preprint

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Background Okadaic acid (OA) is an important liposoluble shellfish toxin distributed worldwide, and mainly responsible for diarrheic shellfish poisoning (DSP) in human beings. It has a variety of toxicities, including cytotoxicity, embryonic toxicity, neurotoxicity, and even genotoxicity. The embryotoxicity of OA is due to it can cross the placental barrier, which was proven in mice. However, there is no direct evidence of its developmental toxicity in human offspring. The chicken (Gallus gallus) embryo is a classic animal model for the studies of early vertebrate embryogenesis and late organogenesis due to its multiple advantages, such as convenience for observation, similarity to mammalian embryo, easy accessibility, and manipulation, etc. Results OA exposure could cause NTDs and inhibit the neuronal differentiation. Immunofluorescent staining demonstrated that OA exposure promoted cell proliferation and inhibit cell apoptosis on the developing neural tube. Besides, the down-regulation of Nrf2 and increases in ROS content and SOD activity in the OA-exposed chicken embryos indicated that OA could result in the generation of oxidative stress in early chick embryos. The inhibition of BMP4 and Shh expression in the dorsal neural tube suggested that OA could also affect the formation of dorsolateral hinge points. The expression of LBP, JUN, FOS, and CCL4 in Toll-like receptor signaling pathway was significantly increased in the OA-exposed embryos, suggesting that the NTDs induced by OA might be associated with Toll-like receptor signaling pathway. Conclusion OA exposure can induce NTDs in chick embryos and increase the incidences of embryo mortality and malformation. Oxidative stress in early chick embryos may be subsequently responsible for the formation of NTDs. OA exposure can affect cell proliferation and apoptosis. Toll-like receptor signaling pathway may be responsible for the NTDs induced by OA.

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“…Many cases of multiple NTDs and severe dysraphism are incompatible with life and death occurs in utero [3]. Hence, most of the earlier information on neurulation was derived from studies in the mouse.…”

Section: Discussionmentioning

confidence: 99%

“…Triple neural tube defect (NTD) is a rare entity with only four cases previously reported in the literature [1–3]. NTDs arise due to the failure of the neural plate to oppose into folds and fuse during neurulation.…”

Section: Introductionmentioning

confidence: 99%

A case report of triple neural tube defect: revisiting the multisite closure theory

et al. 2019

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BackgroundTriple neural tube defects are rare. To the author’s knowledge, there are only four reported cases available in the literature up to date. Controversies exist with regards to the development of neural tube defects. We revisit the multisite closure theory and try to explain the mechanism of neural tube defects in our case.Case presentationWe report a case of one-month-old baby boy who presented to us with three distinct neural tube defects. He had occipital and cervical encephaloceles along with thoracolumbar myelomeningocele accompanied by syrinx and mild hydrocephalus. All the three defects were surgically corrected with good neurological outcome.ConclusionIn the multisite model of human neural tube closure, there are only two fusion sites and two neuropores unlike in mouse. This can explain the origin of open neural tube defects including anencephaly and myelomeningocele (as in our case) but cannot account for the development of encephalocele, which appears to be a post neurulation defect.

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Embryogenesis of triple neural tube defects: sonic hedgehog—a key?

Cited by 5 publications

References 11 publications

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

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

Okadaic acid exposure induced neural tube defects in chicken (Gallus gallus) embryos

A case report of triple neural tube defect: revisiting the multisite closure theory

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