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Ada Weinstock

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Articles by Ada Weinstock

Towards a consensus atlas of human and mouse adipose tissue at single-cell resolution - Nature Metabolism

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By Anne Loft, Margo P. Emont, Ada Weinstock, Allon Wagner, Bart Deplancke, Boxiang Liu, Camilla Scheele, Chenkai Ma, Christian Wolfrum, Clarissa Strieder-Barboza, Congru Li, Elisabet Stener-Victorin, Esti Yeger-Lotem, Farnaz Shamsi, Jiawei Zhong, Joanna Kalucka, Jutta Jalkanen, Katie L Whytock, Kyle D. Dumont, Lauren M. Sparks, Lucas Massier, Luis R. Saraiva, Marc Beyer, Marcelo A. Mori, Mariana Boroni, Martin Walsh, Mary-Elizabeth Patti, Matthias Blüher, Mikael Rydén, Niklas Mejhert, Peng Gao, Rana K. Gupta, Rinki Murphy, Silvia Corvera, Swapan K. Das, Tao Zhang, Theodore Nelson, Timothy E. O’Sullivan, Yu-Hua Tseng, Susanne Mandrup, Erin E. Kershaw, Hannah X. Hui, Nicole L. Solimini
| Nature Verified
Abstract Adipose tissue (AT) is a complex connective tissue with a high relative proportion of adipocytes, which are specialized cells with the ability to store lipids in large droplets. AT is found in multiple discrete depots throughout the body, where it serves as the primary repository for excess calories. In addition, AT has an important role in functions as diverse as insulation, immunity and regulation of metabolic homeostasis.
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Macrophage-to-endothelial cell crosstalk by the cholesterol metabolite 27HC promotes atherosclerosis in male mice - Nature Communications

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By Liming Yu, Lin Xu, Anastasia Sacharidou, Ada Weinstock, Jeffrey McDonald, Erik Nelson, Donald P. McDonnell, Kathryn J. Moore, Edward Fisher, Linzhang Huang, Hsi-hsien Hsieh
| Nature Verified
Abstract Hypercholesterolemia and vascular inflammation are key interconnected contributors to the pathogenesis of atherosclerosis. How hypercholesterolemia initiates vascular inflammation is poorly understood. Here we show in male mice that hypercholesterolemia-driven endothelial activation, monocyte recruitment and atherosclerotic lesion formation are promoted by a crosstalk between macrophages and endothelial cells mediated by the cholesterol metabolite 27-hydroxycholesterol (27HC).
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A wild-type mouse-based model for the regression of inflammation in atherosclerosis

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By Tessa J. Barrett, Michael Peled, Hitoo Nishi, Ada Weinstock
| PLOS
Atherosclerosis can be induced by the injection of a gain-of-function mutant of proprotein convertase subtilisin/kexin type 9 (PCSK9)–encoding adeno-associated viral vector (AAVmPCSK9), avoiding the need for knockout mice models, such as low-density lipoprotein receptor deficient mice. As regression of atherosclerosis is a crucial therapeutic goal, we aimed to establish a regression model based on AAVmPCSK9, which will eliminate the need for germ-line genetic modifications.
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