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. 2017 Mar 27;7:45379. doi: 10.1038/srep45379

Figure 4. PTPIP51 regulated cell function through increasing mitochondrial calcium influx.

Figure 4

(A) Mitochondrial Ca2+ and (B) Cytosolic Ca2+ recordings of neonatal cardiomyocytes transfected with Ad-lacZ or Ad-PTPIP51 in the presence or absence of MCU inhibitor Ru360 (2 μM, for 30 min), in response to caffeine stimulation. n = 41–70 cells in each group for (A) and n = 46–100 cells in each group for (B) from five independent experiments. Bar charts show quantifications of peak amplitude. *P < 0.05versus Ad-lacZ; #P < 0.05 versus Ad-PTPIP51. (C) MCU protein level in sh-MCU-transfected cardiomyocytes. n = 3 independent experiments. *P < 0.05 versus sh-Scramble. (D) Mitochondrial Ca2+ and (E) Cytosolic Ca2+ recordings of neonatal cardiomyocytes transfected with Ad-lacZ, or Ad-PTPIP51 and co-transfected with sh-scramble (sh-Scra) or sh-MCU, in response to caffeine stimulation. n = 35–64 in (D) and n = 54–82 in (E) in each group from five independent experiments. Bar charts show quantifications of peak amplitude. *P < 0.05 versus Ad-lacZ + sh-scramble; #P < 0.05 versus Ad-PTPIP51 + sh-scramble. (F) Annexin V-PI assay by flow cytometry and (G) TUNEL staining in cardiomyocytes transfected with Ad-lacZ or Ad-PTPIP51 with/without Ru360. n = 12 (F) and n = 8 (G) independent experiments. *P < 0.05versus Ad-lacZ; #P < 0.05 versus Ad-PTPIP51.