RIP3 Contributes to Cardiac Hypertrophy by Influencing MLKL-Mediated Calcium Influx

Figure 4

RIP3 is implicated in the MLKL-mediated calcium influx. (a) Co-IP of RIP3 and MLKL in NRCMs stimulated with PE. (b) Western blot showed the cell membrane fraction assay of WT and RIP3^-/- H9c2 cells, RIP3^-/-, RIP3 knockout. WT and RIP3^-/- H9c2 cells were stimulated with Ang-II (1 μM), PE (50 μM), and PBS for 24 hrs. (c) Immunofluorescence of MLKL in WT and RIP3^-/- H9c2 cells stimulated with Ang-II or PE. The same cells in (b) were used. (d) Intracellular calcium concentration of H9c2 cells was determined by Fluo4 staining. The same cells in (c) were stimulated with Ang-II (1 μM) or PE (50 μM) for 24 hrs. (e) The surface area of the indicated NRCM cell lines. Cells were stimulated with Ang-II (1 μM) or PE (50 μM) for 24 hrs. VEC: infected with vector plenti; VEC/shMLKL: infected with vector/shMLKL plenti; oe-RIP3: infected with RIP3 plenti; oe-RIP3/shMLKL: infected with RIP3/shMLKL plenti. kDa: kilo-Dalton; , , and .

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