@article{a736b07a57ef43ce9045232cf089f2a3,
title = "CD81 Controls Beige Fat Progenitor Cell Growth and Energy Balance via FAK Signaling",
abstract = "Adipose tissues dynamically remodel their cellular composition in response to external cues by stimulating beige adipocyte biogenesis; however, the developmental origin and pathways regulating this process remain insufficiently understood owing to adipose tissue heterogeneity. Here, we employed single-cell RNA-seq and identified a unique subset of adipocyte progenitor cells (APCs) that possessed the cell-intrinsic plasticity to give rise to beige fat. This beige APC population is proliferative and marked by cell-surface proteins, including PDGFRα, Sca1, and CD81. Notably, CD81 is not only a beige APC marker but also required for de novo beige fat biogenesis following cold exposure. CD81 forms a complex with αV/β1 and αV/β5 integrins and mediates the activation of integrin-FAK signaling in response to irisin. Importantly, CD81 loss causes diet-induced obesity, insulin resistance, and adipose tissue inflammation. These results suggest that CD81 functions as a key sensor of external inputs and controls beige APC proliferation and whole-body energy homeostasis.",
keywords = "adipocyte progenitors, adipogenesis, beige fat, brown fat, diabetes, metabolic adaptation, metabolic disease, metabolism, obesity, tissue remodeling",
author = "Yasuo Oguri and Kosaku Shinoda and Hyeonwoo Kim and Alba, {Diana L.} and Bolus, {W. Reid} and Qiang Wang and Zachary Brown and Pradhan, {Rachana N.} and Kazuki Tajima and Takeshi Yoneshiro and Kenji Ikeda and Yong Chen and Cheang, {Rachel T.} and Kazuyuki Tsujino and Kim, {Caroline R.} and Greiner, {Vanille Juliette} and Ritwik Datta and Yang, {Christopher D.} and Kamran Atabai and McManus, {Michael T.} and Koliwad, {Suneil K.} and Spiegelman, {Bruce M.} and Shingo Kajimura",
note = "Funding Information: We are grateful to C. Paillart for his support in the CLAMS studies, D. Scheel for histology, and Pollen and Nowakowski for single-cell analysis. This work was supported by the NIH ( DK97441 and DK112268 to S.K., DK110098 to K.A., DK110426 and P30DK026687 to K.S., and 5T32HL007374-38 to H.K.) the Edward Mallinckrodt, Jr. Foundation (to S.K.), the National Center for Advancing Translational Sciences, NIH, through UCSF-CTSI ( UL1 TR000004 to S.K.K.), the JPB Foundation (to B.M.S.), JSPS Overseas Research Fellowships (to Y.O.), the American Diabetes Association ( 1-18-PMF-003 to D.L.A.), the Vera M. Long fellowship (to R.N.P.), the Uehara Memorial Foundation (to T.Y.), and a Larry L. Hillblom Foundation fellowship ( 2019-D-004-FEL to R.D.). Y.O. and K. Tajima were supported by the post-doctoral fellowship from the Manpei Suzuki Diabetes Foundation . Publisher Copyright: {\textcopyright} 2020 Elsevier Inc.",
year = "2020",
month = aug,
day = "6",
doi = "10.1016/j.cell.2020.06.021",
language = "English (US)",
volume = "182",
pages = "563--577.e20",
journal = "Cell",
issn = "0092-8674",
publisher = "Cell Press",
number = "3",
}
