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. 2017 Mar 11;21(9):2068–2076. doi: 10.1111/jcmm.13127

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© 2017 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.

This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

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Schematic representation of the role of PAI1‐PP1 interaction in the regulation of BAD phosphorylation and the anti‐apoptotic effect in endothelial cells. (A) Under stress conditions such as hypoxia–reoxygenation and serum deprivation, PP1 binds to BAD, rendering BAD in an unphosphorylated state and the cell eventually undergoes apoptosis. (B) HP induces BAD phosphorylation and promotes EC survival through promoting the interaction between PAI1 and PP1 and displacing PP1 from complexing with BAD. Activation of Akt signalling also contributes to the phosphorylation of BAD in this process.