Lucy Liaw

Education

  • University of Arizona, 1989, B.S.
  • University of Washington, 1994, Ph.D.
  • Vanderbilt University, 1994-1997, postdoctoral training in Cell Biology, Cardiology

Biosketch

Lucy Liaw has been a research scientist at MaineHealth Institute for Research since 1998. She attended University of Washington, receiving her PhD in Biological Structure/Pathology in 1994 in the area of vascular biology. Her postdoctoral work was in the Dept. Cell Biology at Vanderbilt University, where she studied mouse genetics and cancer biology. She spent one year in the Division of Cardiology at Vanderbilt following her postdoctoral fellowship before joining the faculty at Maine Medical Center. She has academic appointments at UMaine Orono, Tufts University Medical Center, and Univ. Southern Maine. The Liaw laboratory focuses on cardiovascular disease and the impact of obesity and metabolic disease. To study signaling mechanisms, we study cells of the vessel wall (smooth muscle cells, endothelial cells) and the vascular microenvironment (perivascular adipose tissue). We use a variety of cell and molecular approaches, mouse models, and human clinical disease specimens to understand molecular characteristics of disease. In addition, Lucy Liaw is the Director of Research Training and Education Programs at MaineHealth Institute for Research, and oversees our high school, undergraduate, graduate, and postdoctoral training activities. She has extensive experience in peer review at the National Institutes of Health and as a volunteer and advocate for the American Heart Association. As the Principal Investigator of the Center of Biomedical Research Excellence in Mesenchymal and Neural Regulation of Metabolic Networks, she is involved in thematic growth of research in metabolic health at Maine Medical Center via the mentorship of junior investigators and promotion of scientific technologies.

Research Interests

In healthy individuals, perivascular adipose tissue (PVAT) plays a protective role in cardiovascular health by producing factors that suppress inflammation and promote vasodilation. During obesity, however, PVAT expands and loses its vasoprotective activity. Our laboratory goal is to understand adipocyte/vascular interactions at the molecular level by defining the relationship of PVAT to blood vessels under normal conditions and in metabolic disease. This is important because obesity and cardiovascular disease have a high rate of co-occurrence, which is due to multiple molecular and cellular mechanisms. Conversely, we know that dietary interventions that increase cardiovascular health and increase lifespan, such as calorie restriction, also affect the phenotype of PVAT, and increase its thermogenic capacity while reducing lipid accumulation. Using mouse models and dietary modification to either promote obesity or decrease weight gain, we are defining the changes in PVAT that support a disease-susceptible or disease-resistant microenvironment. Parallel studies using human adipose and vascular tissues will help us uncover translational, clinically relevant mechanisms related to human cardiovascular disease.

My laboratory is also in charge of our institutional Mouse Genome Modification Core Facility, which is a resource for the generation of gene targeted and transgenic mouse models of human disease. We provide services from project design to generation of the mouse model and initial characterization, primarily using CRISPR/Cas methods. We aIso provide other mouse-related services such as strain-rederivation, cryopreservation of mouse sperm and embryos, in vitro fertilization, and serving as an institute repository for commonly used mouse strains.

Education and Training Interests

My philosophy is that research training of undergraduate, predoctoral, and postdoctoral scientists is an integral component of a successful laboratory. I am an active member of the Graduate School of Biomedical Science at UMaine Orono, the Tufts University School of Graduate Biomedical Sciences, and the Department of Biological Sciences at University of Southern Maine. I also serve as the Director of Research Training and Education Programs at MHIR, and hold responsibility for postdoctoral fellow and student advising, our responsible conduct of research program, and oversight of our internship and education programs. I also participate in teaching graduate level courses and mentorship for fellowship applications.

Selected Publications

  • Yang X, Yang C, Friesel R, Liaw L. 2022. Sprouty1 has a protective role in atherogenesis and modifies the migratory and inflammatory phenotype of vascular smooth muscle cells. Submitted to ATVB
  • Tero BW, Fortier B, Soucy AN, Paquette G, Liaw L. Quantification of lipid area within thermogenic mouse perivascular adipose tissue using standardized image analysis in FIJI. J Vascular Res 2021, in press.
  • Angueira AR, Sakers AP, Holman CD, Cheng L, Arbocco MN, Shamsi F, Lynes MD, Shrestha R, Okada C, Batmanov K, Susztak K, Tseng Y-H, Liaw L, Seale P. Defining the lineage of thermogenic perivascular adipose tissue. Nat Metab 2021 3(4):469-484.
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    Boucher JM, Ryzhova L, Harrington A, Davis-Knowlton J, Turner JE, Cooper E, Maridas D, Ryzhov S, Rosen CJ, Vary CPH, Liaw L. Pathological conversion of mouse perivascular adipose tissue by Notch activation. Arterioscler, Thromb, Vasc Biol, 2020, 40(9):2227-2243. PMCID: PMC7483939.

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    Dickson D, Stohn P, Rodriguez LS, Hernandez A, Harrington A, Liaw L, Feig LA. Involvement of early embryonic miR-409-3p in the establishment of anxiety levels in female mice. Dev Neurobiol 2020, 80(5-6):160-167.

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    Stieber K, Malka K, Boucher JM, Liaw L. Human perivascular adipose tissue as a regulator of vascular microenvironment and coronary artery and aortic disease. J Cardiology and Cardiovasc Sci 2019, 3(4):10-15. PMCID: PMC7224402.

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    Channabasavaiah G…Liaw L, Miano JM, Burgio G. Reproducibility of CRISPR-Cas9 Methods for generation of conditional mouse alleles: a multi-center evaluation. Genome Biol, 2019, 20(1):171.

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    Scott SS, Yang X, Robich M, Liaw L, Boucher JM. Differentiation capacity of human aortic perivascular adipose progenitor cells. J Vis Exp 2019, 145, e59337, doi:10.3791/59337.

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    Su S, Guntur AR, Nguyen DC, Fakory SS, Doucette CC, Leech C, Lotana H, Kelley M, Kohli J, Martino J, Sims-Lucas S, Liaw L, Vary C, Rosen CJ, Brown AC. A renewable source of human beige adipocytes for development of therapies to treat metabolic syndrome. Cell Reports 2018.

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    Boucher JM, Robich M, Scott SS, Yang X, Ryzhova L, Turner JE, Pinz I, Liaw L. Rab27a regulates human perivascular adipose progenitor cell differentiation. Cardiovascular Drugs and Therapy: PVAT Biology 2018, 32(5):519-530.

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    Peterson SM, Turner JE, Harrington A, Davis-Knowlton J, Lindner V, Gridley T, Vary CPH, Liaw L. Notch2 and proteomic signatures in mouse neointimal lesion formation. Arterio Thromb Vasc Biol 2018, 38(7):1576-1593, NIHMSID 968681.

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    Davis-Knowlton J, Turner JE, Turner A, Damian-Loring S, Hagler N, Henderson T, Emery IF, Duarte CW, Vary CPH, Eldrup-Jorgensen J, Liaw L. Characterization of smooth muscle cells from human atherosclerotic lesions and their responses to Notch signaling. Laboratory Investigation 2018, 38(7):1576-1593.

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    Yang X*, Gong Y, He Q, Licht JD, Liaw L, Friesel RE*. 2018. Loss of Spry1 attenuates vascular smooth muscle proliferation by impairing mitogen-mediated changes in cell cycle regulatory circuits. J Cell Biochem. Apr; 119(4):3267-3279. PMCID:PMC5826877. *: co-corresponding author.

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    Liaw L, Freedman JE, Becker LB, Mehta NN, Liscum L. Peer review practices for evaluating biomedical research grants: a scientific statement from the American Heart Association. Circ Res 2017, 121(4):e9-e19.

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    Bishop KA, Harrington A, Kouranova E, Weinstein EJ, Rosen CJ, Cui X, Liaw L. CRISPR/Cas9 mediated insertion of loxP sites in the mouse Dock7 gene provides an effective alternative to use of targeted embryonic stem cells. G3: Genes, Genomes, Genetics 2016, 6:2051-2061.

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    Liaw L, Prudovsky I, Koza RA, Anunciado-Koza RV, Siviski ME, Lindner V, Friesel RE, Rosen CJ, Baker PR, Simons B, Vary CP. Lipid profiling of in vitro cell models of adipogenic differentiation: relationships with mouse adipose tissues. J Cell Biochem 2016 117:182-193.

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    He Q, Jing H, Liaw L, Gower L, Vary C, Hua S, Yang X. 2016. Suppression of Spry1 inhibits triple-negative breast cancer malignancy by decreasing EGF/EGFR mediate mesenchymal phenotype. Sci Rep; Mar;15(6):23216.

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    Jing H, Liaw L, Friesel R, Vary C, Hua S, Yang X. 2016. Suppression of Spry4 enhances cancer stem cell properties of human MDA-MB-231 breast carcinoma cells. Cancer cell international. 16:19. PMCID: PMC4787021.

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    Rostama B, Turner JE, Seavey GT, Norton CR, Gridley T, Vary CPH, Liaw L. DLL4/Notch1 and BMP9 interdependent signaling induces human endothelial cell quiescence via P27KIP1 and thrombospondin-1. Arter Thromb Vasc Biol 2015, 35(12):2626-2637. PMID: 26471266

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    Rostama B, Peterson SM, Vary CPH, Liaw L. Notch signal integration in the vasculature during remodeling. Vasc Pharmacol 2014, 63:97-104. NIHMSID #636614.

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    Boucher JM, Harrington A, Rostama B, Lindner V, Liaw L. A receptor-specific function for Notch2 in mediating vascular smooth muscle cell growth arrest through p27kip1. Circ Res 2013, 113:975-985. PMCID: PMC3882755.

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    Tang Y, Bai H, Urs S, Wang Z, Liaw L. Notch1 activation in embryonic VE-cadherin populations selectively blocks hematopoietic stem cell generation and fetal liver hematopoiesis. Transgenic Res 2013, 22:403-410. PMCID: PMC3594084.

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    Young K, Conley B, Romero D, Tweedie E, O’Neill C, Pinz I, Brogan L Lindner V, Liaw L, Vary CP. BMP9 regulates endoglin-dependent chemokine responses in endothelial cells. Blood 2012, 120:4263-4273. PMCID:PMC3501721.

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    Urs S, Henderson T, Le P, Rosen CJ, Liaw L. Tissue specific expression of Sprouty1 in mice protects against high fat diet induced fat accumulation, bone loss, and metabolic dysfunction. Br J Nutrition 2012, 6:1-9. NIHMSID #415296.

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    Tang Y, Boucher JM, Liaw L. Histone deacetylase activity selectively regulates Notch-mediated smooth muscle differentiation in human vascular cells. J Amer Heart Assoc 2012, Jun;1(3):e000901, PMCID: PMC3487326.

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    Urs S, Turner B, Tang Y, Rostama B, Small D, Liaw L. Effect of soluble Jagged-1- mediated inhibition of Notch signaling on proliferation and differentiation of an adipocyte progenitor cell model. Adipocyte 2012, 1:46-57.

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    Boucher J, Gridley T, Liaw L. Molecular pathways of Notch signaling in vascular smooth muscle cells. Frontiers in Physiology, 2012, 3:81. PMCID: PMC3151075.

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    Boucher JM, Peterson, SM, Urs S, Zhang C, Liaw L. The miR143/145 cluster is a novel transcriptional target of Jagged-1/Notch signaling in vascular smooth muscle cells. J Biol Chem 2011, 286:28312-28321. PMCID:PMC3151075.

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    Tang Y, Yang X, Friesel RE, Vary CPH, Liaw L. Mechanisms of TGFbeta induced differentiation in human vascular smooth muscle cells. J Vasc Res 2011, 48:485-494. PMCID: PMC3169366.

A complete list of publications can be found on My NCBI

Dissertation Students

Chenhao Yang

Ashley Soucy

 

https://gsbse.umaine.edu/people/caitlin-stieber/

Marissa McGilvrey