@article{065c425c4f194a0ea990850b1be91fa5,
title = "Identification of functionally distinct fibro-inflammatory and adipogenic stromal subpopulations in visceral adipose tissue of adult mice",
abstract = "White adipose tissue (WAT) remodeling is dictated by coordinated interactions between adipocytes and resident stromal-vascular cells; however, the functional heterogeneity of adipose stromal cells has remained unresolved. We combined single-cell RNA-sequencing and FACS to identify and isolate functionally distinct subpopulations of PDGFRβ+ stromal cells within visceral WAT of adult mice. LY6C-CD9-PDGFRβ+ cells represent highly adipogenic visceral adipocyte precursor cells ({\textquoteleft}APCs{\textquoteright}), whereas LY6C+ PDGFRβ+ cells represent fibro-inflammatory progenitors ({\textquoteleft}FIPs{\textquoteright}). FIPs lack adipogenic capacity, display pro-fibrogenic/pro-inflammatory phenotypes, and can exert an anti-adipogenic effect on APCs. The pro-inflammatory phenotype of PDGFRβ+ cells is regulated, at least in part, by NR4A nuclear receptors. These data highlight the functional heterogeneity of visceral WAT perivascular cells, and provide insight into potential cell-cell interactions impacting adipogenesis and inflammation. These improved strategies to isolate FIPs and APCs from visceral WAT will facilitate the study of physiological WAT remodeling and mechanisms leading to metabolic dysfunction.",
author = "Chelsea Hepler and Bo Shan and Qianbin Zhang and Henry, {Gervaise H.} and Mengle Shao and Lavanya Vishvanath and Ghaben, {Alexandra L.} and Mobley, {Angela B.} and Strand, {Douglas W} and Gary Hon and Gupta, {Rana K}",
note = "Funding Information: The authors are grateful to P Scherer for critical reading of the manuscript and members of the UTSW Touchstone Diabetes Center for useful discussions. The authors thank the UTSW Animal Resource Center, Metabolic Phenotyping Core, Pathology Core, Live Cell Imaging Core, Bioinfor-matics Core Facility, Flow Cytometry Core, and McDermott Sequencing Center, for excellent guidance and assistance with experiments performed here. This study was supported by the NIH NIGMS training grant T32 GM008203 and F31DK113696 to CH, NIDDK R01 DK104789 to RKG, the American Heart Association postdoctoral fellowship 16POST26420136 to MS, NIH NIGMS training grant Funding Information: The authors are grateful to P Scherer for critical reading of the manuscript and members of the UTSW Touchstone Diabetes Center for useful discussions. The authors thank the UTSW Animal Resource Center, Metabolic Phenotyping Core, Pathology Core, Live Cell Imaging Core, Bioinformatics Core Facility, Flow Cytometry Core, and McDermott Sequencing Center, for excellent guidance and assistance with experiments performed here. This study was supported by the NIH NIGMS training grant T32 GM008203 and F31DK113696 to CH, NIDDK R01 DK104789 to RKG, the American Heart Association postdoctoral fellowship 16POST26420136 to MS, NIH NIGMS training grant T32 GM008203 to ALG, NIDDK DK098277 and DK110497 to DWS, and CPRIT RR140023, NIGMS DP2GM128203, and Welch Foundation I-1926–20170325 to GCH. Publisher Copyright: {\textcopyright} Hepler et al.",
year = "2018",
month = sep,
doi = "10.7554/eLife.39636",
language = "English (US)",
volume = "7",
journal = "eLife",
issn = "2050-084X",
publisher = "eLife Sciences Publications",
}