Involvement of P38 and ERK1/2 in mitochondrial pathways independent cell apoptosis in oviduct magnum epithelial cells of layers challenged with vanadium

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Abstract

Vanadium (V) can induce cell apoptosis in layers' oviduct resulting in egg quality reduction. In this study, we investigated the relationship between the mitogen-activated protein kinase (MAPK)-signaling pathway and V-induced apoptosis in poultry oviduct magnum epithelial cells (OMECs). Cultured OMECs were divided into 8 treatment groups: 0 μmol/L V (control), 100 μmol/L V (V100), V100 + P38MAPK inhibitor (SB203580), SB203580, V100 + extracellular signal-regulated kinases 1 and 2 (ERK1/2) inhibitor (U0126), U0126, V100 + c-JUN NH2-terminal kinase (JNK) inhibitor (SP600125), and SP600125. The OMECs were pretreated with the MAPK inhibitors before their treatment with V100 for 12 h. V100 increased the apoptosis of OMECs (P

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Wang, J. P., Huang, X. Y., Zhang, K. Y., Ding, X. M., Zeng, Q. F., Bai, S. P., … Mao, X. B. (2018). Involvement of P38 and ERK1/2 in mitochondrial pathways independent cell apoptosis in oviduct magnum epithelial cells of layers challenged with vanadium. Environmental Toxicology, 33(12), 1312–1320. https://doi.org/10.1002/tox.22639

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