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. 2020 Sep 24;31(4):450–462. doi: 10.1038/s41422-020-00411-7

Fig. 6. The pro-proliferative effect of LRP6 knockdown is mediated by the ING5/P21 signaling pathway.

Fig. 6

a The examination of LRP6 protein binding to Ing5 mRNA in NRCMs was performed by RIP assays as described in the schematic diagram. b Quantitation of the decrease in Ing5 mRNA abundance for the control (Ctrl) and si-Lrp6 NRCMs. The dashed lines illustrate the effects of the two parameters on the shape of the curve. Ing5 mRNA was unstable in the absence of LRP6 protein binding. c The ING5, P21, P27, P38 and P53 protein levels were examined in the control (Ctrl) and si-Lrp6 NRCMs. Left, typical western blots, Right, pooled data. The results represent 3–6 experiments. d The P21 protein levels were reduced in the Lrp6-CKO mouse heart tissues and the Ing5 siRNA-treated NRCMs relative to the control (Ctrl) samples. Top, Cre+/− and Lrp6-CKO tissue samples. Bottom, Ctrl and Ing5 siRNA-treated NRCM samples. Left, typical western blots, Right, pooled data. The results represent 3–6 experiments. e EdU assays revealed that the increased proliferation of CMs induced by LRP6 deficiency was attenuated by the overexpression of Ing5. The results represent three experiments. *P < 0.05, ****P < 0.0001, n.s. not significant. Data are presented as means ± SD.