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Evaluation of mesenchymal stem cell contribution to adipose health in the context of high fat diet and exercise (673.2)
Author(s) -
Pincu Yair,
Huntsman Heather,
Zou Kai,
De Lisio Michael,
Mahmassani Ziad,
Boppart Marni
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.673.2
Subject(s) - mesenchymal stem cell , fibrosis , adipose tissue , timp1 , inflammation , mmp2 , endocrinology , medicine , angiogenesis , endurance training , context (archaeology) , mmp9 , gene expression , chemistry , downregulation and upregulation , biology , pathology , gene , biochemistry , cancer , metastasis , paleontology
Objective: To investigate the role of mesenchymal stem cells (MSCs) in adipose tissue (AT) inflammation and fibrosis during high fat diet and exercise training. Methods: C57BL/6 mice were fed high fat (HF, 60%) or low fat (LF, 10%) diets for 8 weeks. Half of the mice were then exercised for 16 weeks. Sca1 + CD45 ‐ MSCs were extracted from epididymal fat, isolated by FACS and analyzed by Q‐PCR. AT inflammation and fibrosis were evaluated using Q‐PCR and histology. Results: HF diet (HFD) increased body weight and exercise attenuated weight gain. AT F4/80, TNFα, and IL‐10 gene expression increased with HF (p<0.05). Exercise did not attenuate this increase. Genes associated with fibrosis (TGFβ1 and Col1α) increased with HFD, and Col1α expression was attenuated with exercise (p<0.05). HFD decreased the percentage of MSCs in AT, but the total number was higher compared to LF fed mice (p<0.05). Exercise did not impact MSC content in AT. MSC gene expression was altered by HFD, but not by exercise. Specifically, Col1α, MMP2, Timp1,VEGFa and IGF‐1 increased while MMP9 decreased (P<0.05). MSC inflammatory gene expression was not altered with HFD or exercise. Conclusion: MSCs do not contribute to AT inflammation, but do express genes necessary for extracellular matrix remodeling and angiogenesis in obese mice. Overall, these data suggest that MSCs provide a mechanism for AT expansion when challenged by HFD.