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. Author manuscript; available in PMC: 2014 May 1.
Published in final edited form as: Circ Heart Fail. 2013 Mar 18;6(3):572–583. doi: 10.1161/CIRCHEARTFAILURE.112.000200

Figure 4. BNIP3 regulates ER and mitochondrial calcium homeostasis.

Figure 4

4-A: BNIP3 overexpression in normal cardiomyocytes significantly decreased beat-to-beat Ca2+ release and ER Ca2+ content with significant increase in Tau, *P<0.05 vs Ad-Null and Ad-Sh BNIP3. There were no differences between the Ad-Null and Ad-Sh BNIP3 treated cardiomyocytes. 4-B: There was threefold increase in mitochondrial Ca2+ in the Ad-BNIP3 group, *P<0.05 vs Ad-Null and Ad-Sh BNIP3. 4-C: In hypertrophic cardiomyocytes, there is robust increase in beat-to-beat Ca2+ release with no change in ER Ca2+ content two weeks after PO, #P<0.05 vs sham. However, five weeks after PO beat-to-beat Ca2+ transients are significantly decreased due to a significant decrease in ER Ca2+ content, *P<0.05 vs all other groups. BNIP3 knockdown significantly increased beat to beat Ca2+ transients and ER Ca2+ content in hypertrophic cardiomyocytes five weeks after PO, &P<0.05 vs POH, W5 + AAV9 Sh Luc 4-D: Mitochondrial Ca2+ significantly increased in hypertrophic cardiomyocytes five weeks after PO, #P<0.05 vs other two groups.