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Mitochondrial Ogg1 prevents loss of mitDNA content, decreases mitochondria fission and apoptosis under conditions of oxidative stress in H9C2 cells
Author(s) -
Torres-Gonzalez Moises,
Gawlowski Thomas,
Scott Brian,
Dillmann Wolfgang
Publication year - 2012
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.26.1_supplement.888.2
Subject(s) - oxidative stress , mitochondrial fission , mitochondrion , apoptosis , microbiology and biotechnology , mitochondrial dna , dna damage , fis1 , dna fragmentation , fragmentation (computing) , cytochrome c , chemistry , biology , mitochondrial fusion , programmed cell death , dna , biochemistry , gene , ecology
Oxidative stress induces damage and depletion of mitochondrial (mit) DNA and suppresses ATP production leading to defects in cell function and initiating cell death. 8‐oxoguanosine DNA glycosylase‐1 (OGG1) acts in the mitochondria to repair DNA damage. In this study H9C2 cells were infected with either adv‐ OGG1 or empty vector and, challenged with menadione, to induce mitochondrial DNA damage. The cells were used to evaluate the effects of OGG1 on mitochondrial DNA content and damage and on apoptotic events induced by oxidative stress. Levels of 8‐oxodG and AP‐sites, metrics of mitochondrial DNA damage, were decreased by 30% and 35%, respectively, in adv‐Ogg1 infected cells. Cells over‐expressing mitOgg1 showed increased membrane potential (p<0.05) and decreased mitochondrial fragmentation (p<0.005). mitOgg1 over‐expression preserved mitDNA content and lowered levels of fission and apoptotic factors such as DRP‐1, FIS1, cytoplasmic cytochrome c, caspase‐3 and caspase‐9. These observations suggest that mitOgg1 may be an alternative to protect cardiac cells against oxidative stress damage.