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Faculty Detail    
Name AIMEE LANDAR
Assistant Professor
 
Campus Address BMR2 506 Zip 2182
Phone 205-975-9507
E-mail landar@uab.edu
Other websites
     

Education
Undergraduate  University of South Alabama    1993  B.M. 
Graduate  University of South Alabama    1998  Ph.D. 


Faculty Appointment(s)
Appointment Type Department Division Rank
Primary  Pathology   Molecular & Cellular Pathology Assistant Professor
Center  Comprehensive Cancer Center  Comprehensive Cancer Center Assistant Professor
Center  Medicine  Comprehensive Diabetes Ctr Assistant Professor
Center  Medicine  Ctr Cardiovasc Bio Assistant Professor

Graduate Biomedical Sciences Affiliations
Cancer Biology 
Molecular and Cellular Pathology Program 
Pathobiology and Molecular Medicine 

Biographical Sketch 
Aimee Landar, Ph.D. is an Assistant Professor at the University of Alabama at Birmingham. She received her Bachelor of Music degree in Flute Performance in 1993, and went on to earn a Ph.D. in Basic Medical Sciences-Pharmacology in 1998 from the University of South Alabama in Mobile, Alabama. Her postdoctoral training began in 1998 at the University of Alabama at Birmingham. She was promoted to Instructor in 2005, and to Research Assistant Professor from 2006-2009. She joined the tenure-earning faculty in 2009 as Assistant Professor.

Society Memberships
Organization Name Position Held Org Link
Society for Free Radical Biology and Medicine  Council Member   

Research/Clinical Interest
Title
Redox signaling and mitochondrial metabolism in disease
Description
The major area of interest of my research program is redox signaling and mitochondrial metabolism. These processes contribute to the control of cell development, differentiation, migration, growth, and death, and are applicable to a broad range of diseases. In the vasculature, endothelial cell redox signaling is important for the upregulation of endogenous antioxidant proteins, such as heme oxygenase-1. Our research has shown that a mitochondrially-targeted electrophile (MTE) which post-translationally modifies specific cysteine residues of metabolic proteins within the mitochondrion, interferes with heme oxygenase-1 upregulation and sensitizes endothelial cells to oxidatively induced cell death. We have also shown that MTEs sensitize breast cancer cells to cell death in response to chemotherapeutic agents. We are exploring the mechanisms by which MTEs mediate cellular responses by analyzing mitochondrial function, adaptation to hypoxia, and upregulation of endogenous antioxidant proteins. In order to accomplish this, we have developed a novel series of MTEs which we are testing in cell and preclinical models of breast cancer. We are using state-of-the-art approaches including a Seahorse extracellular flux analyzer and metabolomics, in combination with proteomic and molecular techniques. We hope to develop these concepts and facilitate their application to the prevention and treatment of human pathologies.

Selected Publications 
Publication PUBMEDID
Diers, A.D.*, Vayalil, P.K.*, Oliva, C.R., Griguer, C.E., Dranka, B.P, Darley-Usmar, V.M., Hurst, D.R., Welch, D.R., Landar, A. Mitochondrial bioenergetics of metastatic breast cancer cells in response to dynamic changes in oxygen tension: Effects of HIF-1α. PLoS One 8(6):e68348, 2013. PMCID:PMC3696014  PMID:23840849 
Wall SB, Oh JY, Diers AR, Landar A. Oxidative modification of proteins: an emerging mechanism of cell signaling. Front Physiol. 3:369 2012 [Epub Sep 14,2012]   PMID:23049513 
Bodenstine, T.M., Vaidya, K.S., Ismail, A., Beck, B.H., Diers, A.R., Edmonds, M.D., Kirsammer, G.T., Landar, A., Welch, D.R. Subsets of ATP-sensitive potassium channel (KATP) inhibitors increase gap junctional intercellular communication in metastatic cancer cell lines independent of SUR expression. FEBS Lett. 586(1):27-31, 2012. PMCID: PMC3249498 [Available on 2013/1/2]  PMID:22119728 
Diers, A.R., Dranka, B.P., Ricart, K.C., Oh, J.Y., Johnson, M.S., Zhou, F., Pallero, M.A., Bodenstine, T., Murphy-Ullrich, J.E., Welch, D.R., Landar, A. Modulation of mammary cancer cell migration by 15-deoxy-Δ12,14-prostaglandin J2: implications for anti-metastatic therapy. Biochem. J. 430(1):69-78, 2010  PMID:20536428 
Diers, A.R., Higdon, A.N., Ricart, K.C., Johnson, M.S., Agarwal, A., Kalyanaraman, B., Landar, A., Darley-Usmar, V.M. Mitochondrial targeting of an electrophile increases apoptotic efficacy via redox cell signaling mechanisms. Biochem. J. 426(1):31-41, 2010.  PMID:19916962 
Ricart, K.C., Bolisetty, S., Johnson, M.S., Perez, J., Agarwal, A., Murphy, M.P., Landar, A. A permissive role of mitochondria in the induction of HO-1 in endothelial cells. Biochem J. 419(2):427-36, 2009.   PMID:19161347 
Oh, J.-Y., Giles, N.M., Landar, A., Darley-Usmar, V. Accumulation of 15-deoxy-delta 12,14-prostaglandin J2 adduct formation with Keap1 over time: effects on potency for intracellular antioxidant defense induction. Biochem J. 411 (2):297-306, 2008.   PMID:18237271 
Gutierrez, J., Ballinger, S.W., Darley-Usmar, V.M., Landar, A. Free radicals, mitochondria, and oxidized lipids: the emerging role in signal transduction in vascular cells. Circ Res. 99(9):924-32, 2006.   PMID:17068300 
Landar, A., Zmijewski, J.W., Dickinson, D.A., Le Goffe, C.L., Johnson, M.S., Milne, G.L., Zanoni, G., Vidari, G., Morrow, J.D., and Darley-Usmar, V.M. The interaction of electrophilic lipid oxidation products with mitochondria in endothelial cells and the formation of reactive oxygen species. Am. J. Physiol. Heart Circ. Physiol. 290(5):H1777-87, 2006.
 
PMID:16387790 
Landar, A., Shiva, S., Levonen, A-L., Oh, J-Y., Zaragoza, C., Johnson, M.S., Darley-Usmar, V.M. Induction of the Permeability Transition and Cytochrome c Release by 15-deoxy Prostaglandin J2 in Mitochondria. Biochem. J. 394(Pt 1):185-195, 2006.   PMID:16268779 

Keywords
redox signaling, cancer, bipolar disorder, atherosclerosis, oxidative stress, mitochondria, metabolic pathways, post-translational modifications