한빛사논문
- 조회507
Seul Gi Lee1,2, Jongbeom Chae1, Seon Min Woo2, Seung Un Seo2, Ha-Jeong Kim3, Sang-Yeob Kim4, David D. Schlaepfer5, In-San Kim6,7, Hee-Sae Park8, Taeg Kyu Kwon2,9 and Ju-Ock Nam1,10
1Department of Food Science and Biotechnology, Kyungpook National University, Daegu 41566, Republic of Korea.
2Department of Immunology, School of Medicine, Keimyung University, Daegu 42601, Republic of Korea.
3Department of Physiology, School of Medicine, Kyungpook National University, Daegu 41944, Republic of Korea.
4ASAN Institute for Life Sciences, ASAN Medical Center, Seoul 05505, Republic of Korea.
5Moores Cancer Center, University of California, San Diego, La Jolla, CA 92093, USA.
6KU-KIST Graduate School of Converging Science and Technology, Korea University, Seoul 02841, Republic of Korea.
7Center for Theragnosis, Biomedical Research Institute, Korea Institute Science and Technology (KIST), Seoul 02792, Republic of Korea.
8School of Biological Sciences and Technology, Chonnam National University, Gwangju 61186, Republic of Korea.
9Center for Forensic Pharmaceutical Science, Keimyung University, Daegu 42601, Republic of Korea.
10Research Institute of Tailored Food Technology, Kyungpook National University, Daegu 41566, Republic of Korea.
Corresponding authors : Correspondence to Taeg Kyu Kwon or Ju-Ock Nam.
Abstract
Extracellular matrix proteins are associated with metabolically healthy adipose tissue and regulate inflammation, fibrosis, angiogenesis, and subsequent metabolic deterioration. In this study, we demonstrated that transforming growth factor-beta (TGFBI), an extracellular matrix (ECM) component, plays an important role in adipose metabolism and browning during high-fat diet-induced obesity. TGFBI KO mice were resistant to adipose tissue hypertrophy, liver steatosis, and insulin resistance. Furthermore, adipose tissue from TGFBI KO mice contained a large population of CD11b+ and CD206+ M2 macrophages, which possibly control adipokine secretion through paracrine mechanisms. Mechanistically, we showed that inhibiting TGFBI-stimulated release of adipsin by Notch-1-dependent signaling resulted in adipocyte browning. TGFBI was physiologically bound to Notch-1 and stimulated its activation in adipocytes. Our findings revealed a novel protective effect of TGFBI deficiency in obesity that is realized via the activation of the Notch-1 signaling pathway.
논문정보
- Research article
- 2023년 03월 (BRIC 등록일 2023-04-11)
- 국내(교신)+국외 연구진
- 생명과학 > 세포생물학
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