The Role of SHIP1 on Apoptosis and Autophagy in the Adipose Tissue of Obese Miceopen access
- Jeong, Jae Hun; Choi, Eun Bee; Jang, Hye Min; Ahn, Yu Jeong; An, Hyeong Seok; Lee, Jong Youl; Park, Gyeongah; Jeong, Eun Ae; Shin, Hyun Joo; Lee, Jaewoong; Kim, Kyung Eun; Roh, Gu Seob
- Issue Date
- SHIP1; macrophage; apoptosis; autophagy; adipose tissue; obesity
- INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, v.21, no.19
- Journal Title
- INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
- Obesity-induced adipocyte apoptosis promotes inflammation and insulin resistance. Src homology domain-containing inositol 5 '-phosphatase 1 (SHIP1) is a key factor of apoptosis and inflammation. However, the role of SHIP1 in obesity-induced adipocyte apoptosis and autophagy is unclear. We found that diet-induced obesity (DIO) mice have significantly greater crown-like structures and terminal deoxynucleotidyl transferase deoxyuridine triphosphate (dUTP) nick-end labeling (TUNEL)-positive cells than ob/ob or control mice. Using RNA sequencing (RNA-seq) analysis, we identified that the apoptosis- and inflammation-related gene Ship1 is upregulated in DIO and ob/ob mice compared with control mice. In particular, DIO mice had more SHIP1-positive macrophages and lysosomal-associated membrane protein 1 (LAMP1) as well as a higher B-cell lymphoma 2 (Bcl-2)-associated X protein (Bax)/Bcl-2 ratio compared with ob/ob or control mice. Furthermore, caloric restriction attenuated adipose tissue inflammation, apoptosis, and autophagy by reversing increases in SHIP1-associated macrophages, Bax/Bcl2-ratio, and autophagy in DIO and ob/ob mice. These results demonstrate that DIO, not ob/ob, aggravates adipocyte inflammation, apoptosis, and autophagy due to differential SHIP1 expression. The evidence of decreased SHIP1-mediated inflammation, apoptosis, and autophagy indicates new therapeutic approaches for obesity-induced chronic inflammatory diseases.
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- College of Medicine > Department of Medicine > Journal Articles
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