Yiliang Chen, PhD
- Versiti Blood Research Institute,
MS, National University of Singapore, Singapore, 2004
BS, Fudan University, China, 2001
Dr. Chen received his Bachelor of Science degree in Genetics from Fudan University (China) in 2001 and his Doctorate degree from the University of Toledo (USA) in 2009, where he studied cholesterol metabolisms and signal transduction. He pursued his postdoctoral work at Blood Center of Wisconsin, Blood Research Institute, where he worked on the functions of a scavenger receptor CD36 and its role in chronic inflammation and atherosclerosis. Dr. Chen joined the MCW faculty in 2020 as an Assistant Professor in the Department of Medicine. He is also a member of MCW’s Cardiovascular Center. Dr. Chen has a life-long passion in the study of metabolic diseases that are often associated with oxidative stress, abnormal lipid metabolism and chronic inflammation.
Honors and Awards
2012 Travel Award for Young Investigators
2008 Retiree’s Scholarship Award Winner, University of Toledo
2004-2009 Pre-Doctoral Fellowship, University of Toledo
2002-2004 Research Fellowship, National University of Singapore, Singapore
We are interested in a chronic inflammatory disease called atherosclerosis, which is the leading cause of death in the developed countries. Atherosclerosis is characterized by atherosclerotic plaques in the medium and large arteries and the major components of the plaques are lipid-laden innate immune cells called macrophages. Using a variety of genetically modified mice as in vivo animal models together with in vitro cell culture model and many biochemical techniques, we study the molecular mechanisms underlying the pro-atherogenic functions of the macrophages.
We are also using novel state-of-the-art technologies including single cell RNA sequencing, high resolution confocal microscopy, Seahorse extracellular flux metabolic assays, GC-MS, and so on to explore cell expression network that are linked to immune activation and metabolic status. With these novel tools, we are able to study not only the macrophage functions but also the cross talk between macrophage and other cell types.
- How CD36-mediated signaling and the fatty acid trafficking influence macrophage immune activation?
- How does mitochondria integrate lipid signals and other metabolic signals to determine its function (e.g. oxidative phosphorylation vs. ROS production)?
- How does macrophage communicate with adipocytes under atherogenic conditions, which facilitate chronic inflammation?
Na/K-ATPase suppresses LPS-induced pro-inflammatory signaling through Lyn.
(Zhang J, Chang J, Beg MA, Huang W, Zhao Y, Dai W, Wu X, Cui W, Pillai SS, Lakhani HV, Sodhi K, Shapiro JI, Sahoo D, Zheng Z, Silverstein RL, Chen Y.) iScience. 2022 Sep 16;25(9):104963 PMID: 36072548 PMCID: PMC9442361 SCOPUS ID: 2-s2.0-85137074779 09/09/2022
AMPK-deficiency forces metformin-challenged cancer cells to switch from carbohydrate metabolism to ketogenesis to support energy metabolism.
(Palma FR, Ratti BA, Paviani V, Coelho DR, Miguel R, Danes JM, Zaichik SV, de Abreu AL, Silva SO, Chen Y, Silverstein RL, Karan U, Jones DP, Bonini MG.) Oncogene. 2021 Sep;40(36):5455-5467 PMID: 34290400 PMCID: PMC8669831 SCOPUS ID: 2-s2.0-85110982210 07/23/2021
CD36 promotes NLRP3 inflammasome activation via the mtROS pathway in renal tubular epithelial cells of diabetic kidneys.
(Hou Y, Wang Q, Han B, Chen Y, Qiao X, Wang L.) Cell Death Dis. 2021 May 21;12(6):523 PMID: 34021126 PMCID: PMC8140121 SCOPUS ID: 2-s2.0-85106615244 05/23/2021
Targeting PIM1-Mediated Metabolism in Myeloid Suppressor Cells to Treat Cancer.
(Xin G, Chen Y, Topchyan P, Kasmani MY, Burns R, Volberding PJ, Wu X, Cohn A, Chen Y, Lin CW, Ho PC, Silverstein R, Dwinell MB, Cui W.) Cancer Immunol Res. 2021 Apr;9(4):454-469 PMID: 33579728 PMCID: PMC8137571 SCOPUS ID: 2-s2.0-85104420312 02/14/2021
Regulation of Na/K-ATPase expression by cholesterol: isoform specificity and the molecular mechanism.
(Zhang J, Li X, Yu H, Larre I, Dube PR, Kennedy DJ, Tang WHW, Westfall K, Pierre SV, Xie Z, Chen Y.) Am J Physiol Cell Physiol. 2020 Dec 01;319(6):C1107-C1119 PMID: 32997514 PMCID: PMC7792677 SCOPUS ID: 2-s2.0-85098226317 10/01/2020
A caveolin binding motif in Na/K-ATPase is required for stem cell differentiation and organogenesis in mammals and C. elegans.
(Wang X, Cai L, Xie JX, Cui X, Zhang J, Wang J, Chen Y, Larre I, Shapiro JI, Pierre SV, Wu D, Zhu GZ, Xie Z.) Sci Adv. 2020 May;6(22):eaaw5851 PMID: 32537485 PMCID: PMC7253156 SCOPUS ID: 2-s2.0-85086625763 06/17/2020
Epithelial and Endothelial Adhesion of Immune Cells Is Enhanced by Cardiotonic Steroid Signaling Through Na+/K+-ATPase-α-1.
(Khalaf FK, Tassavvor I, Mohamed A, Chen Y, Malhotra D, Xie Z, Tian J, Haller ST, Westfall K, Tang WHW, Kennedy DJ.) J Am Heart Assoc. 2020 Feb 04;9(3):e013933 PMID: 32013704 PMCID: PMC7033897 SCOPUS ID: 2-s2.0-85078888113 02/06/2020
Modification of HDL by reactive aldehydes alters select cardioprotective functions of HDL in macrophages.
(Schill RL, Knaack DA, Powers HR, Chen Y, Yang M, Schill DJ, Silverstein RL, Sahoo D.) FEBS J. 2020 Feb;287(4):695-707 PMID: 31386799 PMCID: PMC7002295 SCOPUS ID: 2-s2.0-85070750063 08/07/2019
Mitochondrial Metabolic Reprogramming by CD36 Signaling Drives Macrophage Inflammatory Responses.
(Chen Y, Yang M, Huang W, Chen W, Zhao Y, Schulte ML, Volberding P, Gerbec Z, Zimmermann MT, Zeighami A, Demos W, Zhang J, Knaack DA, Smith BC, Cui W, Malarkannan S, Sodhi K, Shapiro JI, Xie Z, Sahoo D, Silverstein RL.) Circ Res. 2019 Dec 06;125(12):1087-1102 PMID: 31625810 PMCID: PMC6921463 SCOPUS ID: 2-s2.0-85076330129 10/19/2019
Platelet metabolism meets thrombosis.
(Chen Y, Silverstein RL.) Blood. 2018 Sep 13;132(11):1089-1091 PMID: 30213838 SCOPUS ID: 2-s2.0-85053125219 09/15/2018
Cardiotonic Steroids Stimulate Macrophage Inflammatory Responses Through a Pathway Involving CD36, TLR4, and Na/K-ATPase.
(Chen Y, Huang W, Yang M, Xin G, Cui W, Xie Z, Silverstein RL.) Arterioscler Thromb Vasc Biol. 2017 Aug;37(8):1462-1469 PMID: 28619997 PMCID: PMC5532064 SCOPUS ID: 2-s2.0-85020518621 06/18/2017
Platelet CD36 promotes thrombosis by activating redox sensor ERK5 in hyperlipidemic conditions.
(Yang M, Cooley BC, Li W, Chen Y, Vasquez-Vivar J, Scoggins NO, Cameron SJ, Morrell CN, Silverstein RL.) Blood. 2017 May 25;129(21):2917-2927 PMID: 28336528 PMCID: PMC5445574 SCOPUS ID: 2-s2.0-85019661296 03/25/2017