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Autophagy plays a beneficial role against mitochondrial dysfunction in cardiomyocytes
Author(s) -
Dutta Debapriya,
Xu Jinze,
Wohlgemuth Stephanie,
Dunn William A,
Leeuwenburgh Christiaan
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.lb56
Subject(s) - autophagy , microbiology and biotechnology , mitochondrion , viability assay , programmed cell death , apoptosis , mitochondrial dna , biology , cell , chemistry , biochemistry , gene
Healthy mitochondria are vital for cellular homeostasis and survival. Oxidatively stressed mitochondria can release pro‐apoptotic signals causing cell death. Dysfunctional mitochondria are removed by autophagy, a process during which damaged proteins and organelles are sequestered and degraded. Objective To determine whether interventions targeted to upregulate autophagy can protect HL‐1 cardiomyocytes against enhanced mitochondrial damage in HL‐1 cardiomyocytes. Methods HL‐1 cells were treated with the mitochondrial toxin Antimycin A (AMA), and mitochondrial superoxide generation, membrane potential, cellular DNA/RNA oxidation and cell viability were determined. Autophagy was stimulated using amino acid starvation or Rapamycin, and monitored with immunoblotting and epifluorescence imaging. Cell viability was tested with the MTT assay. Results AMA increased mitochondrial superoxide generation, decreased membrane potential, increased cellular DNA/RNA oxidation and decreased cell viability of HL‐1 cells. Both amino acid starvation and Rapamycin increased autophagy in HL‐1 cells, and attenuated AMA‐induced cell death. Conclusion Enhanced autophagy has a beneficial effect on survival of AMA‐treated HL‐1 cells. Research Support: NIH (R01 AG021042 ) to C. Leeuwenburgh and American Heart Fellowship to D. Dutta (10PRE4310091).