Scholars@Duke
Lisheng Zhang

Lisheng Zhang

Assistant Professor in Medicine
Medicine, Cardiology
lisheng.zhang@receptor-biol.duke.edu
Duke Box 3187, Durham, NC 27710
447 Clin Res Lab Bldg, Durham, NC 27710

Selected Publications

Phosphorylation of USP20 on Ser334 by IRAK1 promotes IL-1β-evoked signaling in vascular smooth muscle cells and vascular inflammation.

Journal Article J Biol Chem · July 2023 Reversible lysine-63 (K63) polyubiquitination regulates proinflammatory signaling in vascular smooth muscle cells (SMCs) and plays an integral role in atherosclerosis. Ubiquitin-specific peptidase 20 (USP20) reduces NFκB activation triggered by proinflamma ... Full text Open Access Link to item Cite

Drebrin attenuates atherosclerosis by limiting smooth muscle cell transdifferentiation.

Journal Article Cardiovasc Res · February 21, 2022 AIMS: The F-actin-binding protein Drebrin inhibits smooth muscle cell (SMC) migration, proliferation, and pro-inflammatory signalling. Therefore, we tested the hypothesis that Drebrin constrains atherosclerosis. METHODS AND RESULTS: SM22-Cre+/Dbnflox/flox/ ... Full text Open Access Link to item Cite

Drebrin regulates angiotensin II-induced aortic remodelling.

Journal Article Cardiovasc Res · November 1, 2018 AIMS: The actin-binding protein Drebrin is up-regulated in response to arterial injury and reduces smooth muscle cell (SMC) migration and proliferation through its interaction with the actin cytoskeleton. We, therefore, tested the hypothesis that SMC Drebr ... Full text Open Access Link to item Cite

USP20 (Ubiquitin-Specific Protease 20) Inhibits TNF (Tumor Necrosis Factor)-Triggered Smooth Muscle Cell Inflammation and Attenuates Atherosclerosis.

Journal Article Arterioscler Thromb Vasc Biol · October 2018 Objective- Signaling that activates NFκB (nuclear factor κB) in smooth muscle cells (SMCs) is integral to atherosclerosis and involves reversible ubiquitination that activates proteins downstream of proatherogenic receptors. Deubiquitination of these prote ... Full text Link to item Cite

Interleukin-9 mediates chronic kidney disease-dependent vein graft disease: a role for mast cells.

Journal Article Cardiovasc Res · November 1, 2017 AIMS: Chronic kidney disease (CKD) is a powerful independent risk factor for cardiovascular events, including vein graft failure. Because CKD impairs the clearance of small proteins, we tested the hypothesis that CKD exacerbates vein graft disease by eleva ... Full text Open Access Link to item Cite

The Actin-Binding Protein Drebrin Inhibits Neointimal Hyperplasia.

Journal Article Arterioscler Thromb Vasc Biol · May 2016 OBJECTIVE: Vascular smooth muscle cell (SMC) migration is regulated by cytoskeletal remodeling as well as by certain transient receptor potential (TRP) channels, nonselective cation channels that modulate calcium influx. Proper function of multiple subfami ... Full text Open Access Link to item Cite

Ubiquitin-specific Protease 20 Regulates the Reciprocal Functions of β-Arrestin2 in Toll-like Receptor 4-promoted Nuclear Factor κB (NFκB) Activation.

Journal Article J Biol Chem · April 1, 2016 Toll-like receptor 4 (TLR4) promotes vascular inflammatory disorders such as neointimal hyperplasia and atherosclerosis. TLR4 triggers NFκB signaling through the ubiquitin ligase TRAF6 (tumor necrosis factor receptor-associated factor 6). TRAF6 activity ca ... Full text Link to item Cite

Kruppel-like factor 15 is critical for vascular inflammation.

Journal Article J Clin Invest · October 2013 Activation of cells intrinsic to the vessel wall is central to the initiation and progression of vascular inflammation. As the dominant cellular constituent of the vessel wall, vascular smooth muscle cells (VSMCs) and their functions are critical determina ... Full text Open Access Link to item Cite

Kalirin promotes neointimal hyperplasia by activating Rac in smooth muscle cells.

Journal Article Arterioscler Thromb Vasc Biol · April 2013 OBJECTIVE: Kalirin is a multifunctional protein that contains 2 guanine nucleotide exchange factor domains for the GTPases Rac1 and RhoA. Variants of KALRN have been associated with atherosclerosis in humans, but Kalirin's activity has been characterized a ... Full text Open Access Link to item Cite

Vein graft neointimal hyperplasia is exacerbated by CXCR4 signaling in vein graft-extrinsic cells.

Journal Article J Vasc Surg · November 2012 OBJECTIVE: Because vein graft neointimal hyperplasia engenders vein graft failure, and because most vein graft neointimal cells derive from outside the vein graft, we sought to determine whether vein graft neointimal hyperplasia is affected by activity of ... Full text Open Access Link to item Cite

G protein-coupled receptor kinase-5 attenuates atherosclerosis by regulating receptor tyrosine kinases and 7-transmembrane receptors.

Journal Article Arterioscler Thromb Vasc Biol · February 2012 OBJECTIVE: G protein-coupled receptor kinase-5 (GRK5) is a widely expressed Ser/Thr kinase that regulates several atherogenic receptors and may activate or inhibit nuclear factor-κB (NF-κB). This study sought to determine whether and by what mechanisms GRK ... Full text Open Access Link to item Cite

Human umbilical cord blood-derived endothelial cells reendothelialize vein grafts and prevent thrombosis.

Journal Article Arterioscler Thromb Vasc Biol · November 2010 OBJECTIVE: To accelerate vein graft reendothelialization and reduce vein graft thrombosis by infusing human umbilical cord blood-derived endothelial cells (hCB-ECs) because loss of endothelium contributes to vein graft thrombosis and neointimal hyperplasia ... Full text Open Access Link to item Cite

Human umbilical cord blood endothelial progenitor cells decrease vein graft neointimal hyperplasia in SCID mice.

Journal Article Atherosclerosis · September 2010 AIMS: Vein graft endothelial damage is a key step in the development of neointimal hyperplasia, leading to vein graft failure. We sought to determine whether exogenous endothelial progenitor cells could promote vein graft re-endothelialization, and thereby ... Full text Open Access Link to item Cite

Aging-related atherosclerosis is exacerbated by arterial expression of tumor necrosis factor receptor-1: evidence from mouse models and human association studies.

Journal Article Hum Mol Genet · July 15, 2010 Aging is believed to be among the most important contributors to atherosclerosis, through mechanisms that remain largely obscure. Serum levels of tumor necrosis factor (TNF) rise with aging and have been correlated with the incidence of myocardial infarcti ... Full text Open Access Link to item Cite

Neuropeptide Y gene polymorphisms confer risk of early-onset atherosclerosis.

Journal Article PLoS Genet · January 2009 Neuropeptide Y (NPY) is a strong candidate gene for coronary artery disease (CAD). We have previously identified genetic linkage to familial CAD in the genomic region of NPY. We performed follow-up genetic, biostatistical, and functional analysis of NPY in ... Full text Open Access Link to item Cite

Beta-arrestins regulate atherosclerosis and neointimal hyperplasia by controlling smooth muscle cell proliferation and migration.

Journal Article Circ Res · July 3, 2008 Atherosclerosis and arterial injury-induced neointimal hyperplasia involve medial smooth muscle cell (SMC) proliferation and migration into the arterial intima. Because many 7-transmembrane and growth factor receptors promote atherosclerosis, we hypothesiz ... Full text Open Access Link to item Cite

Tumor necrosis factor receptor-2 signaling attenuates vein graft neointima formation by promoting endothelial recovery.

Journal Article Arterioscler Thromb Vasc Biol · February 2008 OBJECTIVE: Inflammation appears intricately linked to vein graft arterialization. We have previously shown that tumor necrosis factor (TNF) receptor-1 (TNFR1, p55) signaling augments vein graft neointimal hyperplasia (NH) and remodeling through its effects ... Full text Link to item Cite

Expression of tumor necrosis factor receptor-1 in arterial wall cells promotes atherosclerosis.

Journal Article Arterioscler Thromb Vasc Biol · May 2007 OBJECTIVE: Mechanisms by which tumor necrosis factor-alpha (TNF) contributes to atherosclerosis remain largely obscure. We therefore sought to determine the role of the arterial wall TNF receptor-1 (TNFR1) in atherogenesis. METHODS AND RESULTS: Carotid art ... Full text Link to item Cite

Human cord blood endothelial progenitors decrease neointimal hyperplasia in SCID mouse vein grafts

Conference JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY · March 6, 2007 Link to item Cite

Regulation of the platelet-derived growth factor receptor-beta by G protein-coupled receptor kinase-5 in vascular smooth muscle cells involves the phosphatase Shp2.

Journal Article J Biol Chem · December 8, 2006 Smooth muscle cell (SMC) proliferation and migration are substantially controlled by the platelet-derived growth factor receptor-beta (PDGFRbeta), which can be regulated by the Ser/Thr kinase G protein-coupled receptor kinase-2 (GRK2). In mouse aortic SMCs ... Full text Link to item Cite

Activation of vascular smooth muscle cells by TNF and PDGF: overlapping and complementary signal transduction mechanisms.

Journal Article Cardiovasc Res · February 15, 2005 OBJECTIVE: Because tumor necrosis factor-alpha (TNF) has been implicated in the pathogenesis of vein graft neointimal hyperplasia, we sought to determine mechanisms by which TNF could induce proliferative and migratory responses in smooth muscle cells (SMC ... Full text Link to item Cite

Vein graft neointimal hyperplasia is exacerbated by tumor necrosis factor receptor-1 signaling in graft-intrinsic cells.

Journal Article Arterioscler Thromb Vasc Biol · December 2004 OBJECTIVE: Vein graft remodeling and neointimal hyperplasia involve inflammation, graft-intrinsic cells, and recruitment of vascular progenitor cells. We sought to examine if the inflammatory cytokine tumor necrosis factor (TNF) affects vein graft remodeli ... Full text Link to item Cite

Graft-extrinsic cells predominate in vein graft arterialization.

Journal Article Arterioscler Thromb Vasc Biol · March 2004 OBJECTIVE: Vein graft disease involves neointimal smooth muscle cells, the origins of which are unclear. This study sought to characterize and quantitate vein graft infiltration by cells extrinsic to the graft in a mouse model of vein graft disease. METHOD ... Full text Link to item Cite

Neointimal hyperplasia rapidly reaches steady state in a novel murine vein graft model.

Journal Article J Vasc Surg · October 2002 OBJECTIVE: Neointimal hyperplasia remains a principal cause of vein graft failure. Genetic contributions to vein graft neointimal hyperplasia could be well studied in the mouse; however, surgical approaches to vein bypass surgery in the mouse have yet to r ... Link to item Cite

Overexpression of G protein-coupled receptor kinase-2 in smooth muscle cells reduces neointimal hyperplasia.

Journal Article J Mol Cell Cardiol · October 2002 The activation of vascular smooth muscle cells (SMCs) in neointimal hyperplasia involves signaling through receptor tyrosine kinases as well as G protein-coupled receptors. Overexpression of G protein-coupled receptor kinase-2 (GRK2) in SMCs can attenuate ... Full text Link to item Cite