Mei-Zhen Cui

Mei-Zhen Cui

Professor, Co-director of Biomedical Research Center
Biology Program
College of Arts and Sciences
Department of Biology
Office
ST 2254

Department of Biology 

College of Arts and Sciences

 

Education

  • B.S., Jilin University, Changchun, China, 1982, Chemistry
  • M.S., Jilin University, Changchun, China, 1985, Biochemistry
  • Ph.D., Tokyo Institute of Technology, Japan, 1990, Molecular Biology


Professional Experience

  • Postdoctoral Fellow, The Scripps Research Institute, California, 1990-1994, Vascular Biology.
  • Research Associate, Cleveland Clinic Foundation, Ohio, 1995-1999, Vascular Biology

Teaching & Training

  • Graduate Course: Vascular cell signaling; Molecular mechanisms of vascular disease
  • Training undergraduate/graduate students and postdoctoral fellows

Selected Awards/Honors and Positions

  • 1998 Scientist Development Award from the American Heart Association
  • 2002 Pfizer Basic Research Award
  • 2003 American Heart Association Research Award (GIA)
  • 2004 Philip Morris Research Award
  • 2006 The University of Tennessee Chancellor’s Award for Research and Creative Achievement
  • 2010 RayBiotechnology Inc Research Award
  • 2013– Editorial Board, Journal of Biological Chemistry
  • 2018 University of Texas System STAR Award 

Research Interests

  • Phospholipid interaction with vascular cells
  • Smooth muscle cell proliferation and migration
  • Endothelial cell dysfunction
  • Foam cell formation
  • Macrophage migration
  • Gene expression
  • Signal transduction
  • Matricellular protein function

The research goal of my laboratory is to understand molecular mechanisms
underlying vascular diseases, such as atherosclerosis, restenosis and thrombosis.
The focus of our research is to investigate vascular diseases caused by aberrant
signaling mechanisms, including extracellular molecule interaction with cell
membrane receptors, signal transduction pathways, gene transcription and
protein modification. We integrate molecular, cellular and genetic approaches to
discover the mechanisms that control the progression of vascular disease.

Selected Recent Publications: 

  • Hao, F., Tan, M., Xu, X., and Cui, M.-Z., Histamine Induces Egr-1 Expression
    in Human Aortic Endothelial Cells via the H1 Receptor-mediated Protein
    Kinase Cd-Dependent ERK Activation Pathway, J. Biol. Chem, 2008, 283(40):
    26928–26936.
  • Tan, M., Hao, F., Xu, X., Chisolm, G. and Cui, M.-Z.,
    Lysophosphatidylcholine activates a novel PKD2-mediated signaling pathway
    that controls monocytic THP-1 cell migration, Arterioscler Thromb Vasc Biol.,
    2009, 29:1376-1382.
  • Hao, F. Tan, M. Wu, D. Xu, X. and Cui, M.-Z., Lysophosphatidic acid
    induction of interleukin 6 secretion from aortic smooth muscle cells via LPA1
    regulated, PKC dependent and p38alpha mediated pathway, American Journal
    of Physiology-Heart and Circulatory Physiology, 2010, 298(3):H974-83.
  • Wang, Kan; Cai, Lei; Hao, Feng; Xu, Xuemin; Cui, M.-Z.; Wang, Shanfeng,
    Distinct Cell Responses to Substrates Consisting of Poly(ε-caprolactone) and
    Poly(propylene fumarate) in the Presence or Absence of Crosslinks.
    Biomacromolecules, 2010,11(10):2748-59.
  • Cui, M.-Z., (review) Lysophosphatidic acid effects on atherosclerosis and
    thrombosis. Clinical Lipidology, 2011, 6(4), 413-426.
  • Takuya, I., Zhang, F., Sun, L., Hao, F., Schmitz, C., Xu, X. and Cui, M.-Z.,
    Lysophosphatidic Acid Induces Early Growth Response-1 (Egr-1) Protein
    Expression via Protein Kinase Cδ-regulated Extracellular Signal-regulated
    Kinase (ERK) and c-Jun N-terminal Kinase (JNK) Activation in Vascular
    Smooth Muscle Cells. J. Biol. Chem. 2012, 287: 22635-22642.
  • Zeng L, Li T, Xu DC, Liu J, Cui M.-Z, Fu X, Xu X. Death Receptor 6 Induces
    Apoptosis Not through Thype I or Type II Pathways, but via a Unique
    Mitochondria-dependent Pathway by Interacting with Bax Protein. J. Biol.
    Chem. 2012, 287(34):29125-33.
  • Mao, G, Cui M.-Z, Li, T, Jin, Y, Xu, X. Pen-2 is dispensable for
    endoproteolysis of presenilin 1, and nicastrin-Aph subcomplex is important for
    both γ-secretase assembly and substrate recruitment. J. Neurochem.
    2012,123(5):837-44.
  • Hao, F., Wu, D. Xu, X. and Cui, M.-Z.,Histamine induces activation of protein
    kinase D that mediates tissue factor expression and activity in human aortic
    smooth muscle cells. American Journal of Physiology-Heart and Circulatory
    Physiology, 2012, 303(11):H1344-52.
  • Shi, J., Dong, Y., Cui, M.-Z. and Xu, X., Lysophosphatidic acid induces
    increased BACE1 expression and Abeta formation, Accepted for publication
    on Biochim Biophys Acta- Molecular Basis of Disease, 2013, 1832(1):29-38.
  • Li, Ting, Zeng, L., Gao, W., Cui, M.-Z., Fu, X. and Xu, X. PSAP induces a
    unique Apaf-1 and Smac-dependent mitochondrial apoptotic pathway
    independent of Bcl-2 family proteins. Biochim Biophys Acta- Molecular Basis
    of Disease. 2013, 1832(3):453-74.
  • Wu, DD, Zhang, F, Hao, F, Chun, J, Xu, X and Cui, M.-Z., Matricellular
    Protein Cyr61 Bridges Lysophosphatidic Acid and Integrin Pathways Leading
    to Cell Migration, J. Biol. Chem. 2014, 289(9): 5774-5783.
  • Kimura, TE, Hindmarch, CC, Hewer, RC, Cui, M.-Z., Newby, AC and Bond,
    M., Inhibition of Egr1 expression underlies the anti-mitogenic effects of cAMP
    in vascular smooth muscle cells, J Mol Cell Cardiol. 2014, Jul;72:9-19.
  • Zhang, F., Hao, F., An, D., Zeng, L., Wang, Y., Xu, X., and Cui, M.-Z.,
    Matricellular Protein Cyr61 Is a Key Mediator of Platelet-derived Growth
    Factor-induced Cell Migration, J. Biol. Chem. 2015, 290(13): 8232–8242.
  • Zeng, L., Hu, C., Zhang, F., Xu, DC., Cui, M. Z., and Xu, X., FLIP and PSAP
    Mediate Presenilin 1-induced γ-secretase dependent and independent apoptosis
    respectively. J Biol Chem. 2015, 24;290(30):18269-80.
  • Cui, M. Z., (Editorial Focus) Potential therapeutics for myocardial ischemiareperfusion
    injury. Focus on "Induction of cardioprotection by small netrin-1
    derived peptides". American Journal of Physiology - Cell Physiology. 2015 Jul
    15;309(2):C97-9.
  • Hu C, Zeng L, Li T, Meyer MA, Cui M.-Z, Xu X, Nicastrin is required for
    APP but not Notch processing, while Aph-1 is dispensable for processing of
    both APP and Notch. J Neurochem. 2016,136, 1246-1258
  • Huang, Y., Wang, Y., Tan L., Sun, L., Petrosino, J., Cui, M.-Z., Hao, F. and
    Zhang, M., Nanospherical arabinogalactan proteins are a key component of the
    high-strength adhesive secreted by English Ivy, Proc Natl Acad Sci U S A.
    2016, Jun 7;113(23): E3193-202.
  • Hao, F., Zhang, F., Wu, D. D., An, D., Shi, J., Li, G., Xu, X. and Cui, M.-Z.
    Lysophosphatidic acid-induced vascular neointimal formation in mouse carotid
    arteries is mediated by the matricellular protein CCN1/Cyr61. American
    Journal of Physiology- Cell Physiology. 2016 Dec 1;311(6):C975-C984.
    PMID: 27760754.
  • Dou, Q., Hao, F., Sun, L., Xu, X. and Cui, M.-Z. CREB and SRF mediate
    LPA-induced CCN1 expression in vascular smooth muscle cells. Canadian
    Journal of Physiology & Pharmacology. 2017 Mar;95(3):275-280. Doi:
    10.1139/cjpp-2016-0559, PMID:28157379
  • Hu, C., Xu, J., Zeng, L., Li, T., Cui, M.-Z., and Xu, X. Pen-2 and presenilin are
    sufficient to catalyze Notch processing. Journal of Alzheimer’s Disease. 2017;
    56 (4), 1263-1269. PMID: 28234257
  • Dong Y., Wu, Y., Cui, M.-Z., and Xu, X. Lysophosphatidic acid triggers
    apoptosis in HeLa cells through the upregulation of tumor necrosis actor
    receptor superfamily member 21, Mediators Inflamm. 2017; 2017:2754756.
    doi: 10.1155/2017/2754756. PMID:28348459. PMCID: PMC5350427.
  • An, D., Hao, F., Zhang, F., Kong, W., Xu, X. and Cui, M.-Z. CD14 Is a Key
    Mediator of Both Lysophosphatidic Acid and Lipopolysaccharide Induction of
    Foam Cell Formation. J. Biol. Chem. 2017, Sep 1; 292(35):14391-14400. doi:
    10.1074/jbc.M117.781807. Epub 2017 Jul 13. PMID: 28705936.
  • Jin, R., Xiao, A.Y., Song, Z., Yu, S., Li, J., Cui, M.-Z., Li, G., Platelet CD40
    Mediates Leukocyte Recruitment and Neointima Formation after Arterial
    Denudation Injury in Atherosclerosis-Prone Mice. Am. J. Pathol., 2017 Oct 14.
    pii: S0002-9440(17)30009-3. doi: 10.1016/j.ajpath.2017.09.007.
    PMID:29037856
  • An, D., Hao, F., Hu, C., Kong, W., Xu, X. and Cui, M.-Z. JNK1 mediates
    lipopolysaccharide-induced CD14 and SR-AI expression and macrophage
    foam cell formation. Front Physiol. 2018 Jan 5;8:1075. doi:
    10.3389/fphys.2017.01075. PMID: 29354064