![Leonard Anderson, Ph.D.](/_resources/MSMimages/FacultyDirectoryImages/Medicine/LeonardAndersonRV.jpg)
Leonard Anderson, Ph.D.
Assistant Professor
Physiology
Cardiovascular Research Institute
Location: Research Wing 210
Phone: 404-756-8921
E-mail: landerson@msm.edu
Education
GRADUATE:Northwestern Medical School
Degree: Doctor of Philosophy in Molecular Genetics
UNDERGRADUATE:
Southern Illinois University-Carbondale
Degree: Bachelor of Science in Microbiology and Chemistry
Research Interests
Vascular diseases involving hyperproliferation of VSMCs, such as atherosclerosis, is one of the major causes of mortality in the U.S. and one of the leading causes of mortality among African Americans. VSMCs play a critical role in early vasculogenesis and blood vessel maintenance. The requirement for VSMC replenishment after vessel injury by putative stem cell progenitors suggest unique changes in the cellular transcriptome when compared to other cell lineages such as neurons, skeletal muscle, and cardiomyocytes. Our lab is currently interested in defining the process by which pluripotent stem cells become VSMCs at the transcriptional and, hence, signal transduction level by utilizing various innovative genomics technologies (i.e. Agilent OligoArrays, Affymetrix GeneChips, and protein arrays) to identify novel genes and proteins that play a crucial role in early VSMC fate determination. We are functionally characterizing these genes in pluripotent mouse embryonal carcinoma stem cells (P19) and various clonal derivatives by utilizing either 'gain of-' or 'loss of-' function methodologies to alter expression levels of identified genes. These functional genomics studies will provide insight into the mechanism(s) by which specific genes are involved in early cell lineage determination within the vasculature. Although the therapeutic potential of ES cell-derived ex vivo therapy has been demonstrated in mouse models of atherosclerosis and restenosis after balloon angioplasty, the outcome of these studies suggest further understanding of the basic molecular mechanisms involved in this process is required. The outcome of our genomic studies will allow us to gain insight into these early signaling events and potentially generate modified ES cells with a predetermined VSMC, and thus, greater therapeutic efficacy in vivo.Publications
Anderson LM, Gibbons GH. Notch: a mastermind of vascular morphogenesis. J Clin Invest. 2007 Feb;117(2):299-302. PMID: 17273550
Morello F, de Boer RA, Steffensen KR, Gnecchi M, Chisholm JW, Boomsma F, Anderson LM, Lawn RM, Gustafsson JA, Lopez-Ilasaca M, Pratt RE, Dzau VJ. Liver X receptors alpha
and beta regulate renin expression in vivo. J Clin Invest. 2005 Jul;115(7):1913-22. PMID: 16007255
Anderson LM, Choe SE, Yukhananov RY, Hopfner RL, Church GM, Pratt RE, Dzau VJ. Identification
of a novel set of genes regulated by a unique liver X receptor-alpha -mediated transcription
mechanism. J Biol Chem. 2003 Apr 25;278(17):15252-60. Epub 2003 Jan 27. PMID: 12551904
Loguinov AV, Anderson LM, Crosby GJ, Yukhananov RY. Gene expression following acute morphine administration. Physiol Genomics. 2001 Aug 28;6(3):169-81. PMID: 11526201
Sidiropoulos P, Liu H, Mungre S, Anderson L, Thimmapaya B, Pope RM. Efficacy of adenoviral TNF alpha antisense is enhanced by
a macrophage specific promoter. Gene Ther. 2001 Feb;8(3):223-31. PMID: 11313794
Anderson LM, Krotz S, Weitzman SA, Thimmapaya B. Breast cancer-specific expression of the Candida
albicans cytosine deaminase gene using a transcriptional targeting approach. Cancer Gene Ther. 2000 Jun;7(6):845-52. PMID: 10880014
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