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Intravenous mesenchymal stem cell administration spurs endogenous hepatic mitochondrial gene expression in the diet‐induced obese mouse (693.10)
Author(s) -
Newell Christopher,
Hughey Curtis,
Pihl Carin,
Hittel Dustin,
Shearer Jane
Publication year - 2014
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.28.1_supplement.693.10
Subject(s) - endogeny , mesenchymal stem cell , oxidative stress , glyceraldehyde 3 phosphate dehydrogenase , paracrine signalling , biology , mitochondrion , oxidative phosphorylation , endocrinology , cell , medicine , gene expression , microbiology and biotechnology , gene , biochemistry , receptor
Intravenous human mesenchymal stem cell (MSC) administration alleviates hepatic oxidative stress in the diet‐induced obese mouse. However, the underlying mechanisms responsible for these benefits are uncertain. Possible explanations range from direct cell engraftment to paracrine‐mediated endogenous cell stimulation. To examine this question, male C57BL/J mice (n=24) were assigned to one of two dietary groups; chow (10% kcal fat) and high fat (60% kcal fat) for 12 wk. Animals were further divided, receiving intravenous saline (0.2 mL PBS) or MSC (750,000 cells). Post‐injection (24 h), qRT‐PCR was used to identify changes in endogenous (mouse) and exogenous (human) transcripts for glyceraldehyde 3‐phosphate dehydrogenase (GAPDH) and mouse mitochondrial protein cytochrome c oxidase subunit II (COX‐II) in the liver. Human GAPDH and COX‐II were detected in the livers of animals undergoing MSC treatment indicating successful cell targeting. Declines in mouse COX‐II caused by HF were mitigated by MSC therapy (p<0.05). Results indicate that MSC administration triggers endogenous mitochondrial gene proliferation which may explain the ability of MSC to mitigate hepatic oxidative stress in diet‐induced obesity. Grant Funding Source : Supported by MitoCanada