Imidacloprid exposure suppresses neural crest cells generation during early chick embryo development

Chao-Jie Wang, Guang Wang, Xiao-yu Wang, Meng Liu, Manli Chuai, Kenneth Ka Ho Lee, Xiao-Song He, Da-Xiang Lu, Xuesong Yang (Lead / Corresponding author)

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    33 Citations (Scopus)


    Imidacloprid is a neonicotinoid pesticide that is widely used in the control pests found on crops and fleas on pets. However, it is still unclear whether imidacloprid exposure could affect early embryo development-despite some studies having been conducted on the gametes. In this study, we demonstrated that imidacloprid exposure could lead to abnormal craniofacial osteogenesis in the developing chick embryo. Cranial neural crest cells (NCCs) are the progenitor cells of the chick cranial skull. We found that the imidacloprid exposure retards the development of gastrulating chick embryos. HNK-1, PAX7, and Ap-2α immunohistological stainings indicated that cranial NCCs generation was inhibited after imidacloprid exposure. Double immunofluorescent staining (Ap-2α and PHIS3 or PAX7 and c-Caspase3) revealed that imidacloprid exposure inhibited both NCC proliferation and apoptosis. In addition, it inhibited NCCs production by repressing Msx1 and BMP4 expression in the developing neural tube and by altering expression of EMT-related adhesion molecules (Cad6B, E-Cadherin, and N-cadherin) in the developing neural crests. We also determined that imidacloprid exposure suppressed cranial NCCs migration and their ability to differentiate. In sum, we have provided experimental evidence that imidacloprid exposure during embryogenesis disrupts NCCs development, which in turn causes defective cranial bone development.

    Original languageEnglish
    Pages (from-to)4705-4715
    Number of pages11
    JournalJournal of Agricultural and Food Chemistry
    Issue number23
    Early online date19 May 2016
    Publication statusPublished - 15 Jun 2016


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