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Professor |
Training
• M.S., Biology, 1980, Warsaw University, Warsaw, Poland
• Ph.D., Genetics, Institute of Biochemistry and Biophysics, Polish Academy of Sciences, Warsaw, Poland
• Postdoctoral Fellow, University of Arkansas for Medical Sciences, Little Rock, Arkansas
Appointments
• Postdoctoral Fellow, Department of Genetics, Institute of Biochemistry and Biophysics, Polish Academy
of Sciences, Warsaw, Poland, 1985-1988
• Research Associate and Adjunct, Department of Genetics, Institute of Biochemistry and Biophysics,
Polish Academy of Sciences, Warsaw, Poland, 1988-1990
• Postdoctoral Fellow, Department of Internal Medicine, Division of Gerontology, University of Arkansas
for Medical Sciences (UAMS), Little Rock Arkansas, 1991-1995
• Research Assistant Professor, Department of Geriatrics and Reynolds Center on Aging, UAMS, Little
Rock, Arkansas, 1995-2004
• Faculty Member of the Arkansas Cancer Research Center, UAMS, Little Rock, Arkansas, 2003-2007
• Associate Professor, Geriatric Research (non-tentured track), Department of Geriatrics and Reynolds
Institute on Aging, UAMS, Little Rock, Arkansas, 2005-2007
• Professor, Department of Orthopaedic Surgery with a joint appointment in the Department of
Physiology & Pharmacology, University of Toledo College of Medicine, Health Science Campus,
Toledo, Ohio, 2007-
Research Interests:
Diabetes, obesity, and osteoporosis are major public health concerns due to their prevalence in our increasingly sedentary and aging society. The peroxisome proliferator-activated receptor-gamma (PPARg) transcription factor is a protein that regulates glucose metabolism and energy expenditure. This protein also regulates lineage commitment of bone marrow mesenchymal stem cells (MSC). PPARg protein is a target for a class of anti-diabetic drugs TZDs, which decrease glucose levels and increase insulin sensitivity. Although their beneficial anti-diabetic profile, prolonged treatment with these drugs leads to the bone loss and increased number of bone fractures in diabetic patients. Dr. Lecka-Czernik's research has demonstrated that TZDs affect bone mass by changing lineage commitment of MSC toward formation of fat cells (adipocytes) and away from formation of bone forming cells (osteoblast). As a result, TZD administration to animals, as well as to humans, leads to the bone loss and the gain of fat in the bone marrow. Her research also demonstrated that the similar mechanism involving PPARg protein is responsible for bone loss with aging.
Ongoing research projects:
1. Development of an animal model of therapeutic intervention to prevent TZD-associated bone loss.
2. Improve bone fracture healing in diabetic patients by means of stem cell-based and siRNA-based therapies.
3. Determine age- and diabetes-related mechanisms which decrease MSC potential to regenerate bone.
Selected Publications
• Rzonca, S.O., Suva, L.J., Gaddy, D., Montague, D.C., Lecka-Czernik, B. Bone is a target for the
anti-diabetic compound rosiglitazone, Endocrinology 145:401-406, 2004.
• Moerman, E.J., Teng, K., Lipschitz, D.A. and Lecka-Czernik, B. Aging activates adipogenic and
suppresses osteogenic programs in mesenchymal marrowstroma/stem cells: A role of PPAR-γ2
transcription factor and TGF-β/BMP signaling pathways. Aging Cell 3:379-389, 2004.
• Lazarenko, O.P., Rzonca, S.O., Suva, L.J., Lecka-Czernik, B. Netoglitazone is a PPAR-gamma
ligand with selective effects on bone and fat. Bone 38:74-84, 2006.
• Schwartz, A.V., Sellmeyer, D.E., Vittinghoff, E., Palermo, L., Lecka-Czernik, B., Kenneth R. Feingold,
K.R., Strotmeyer, E.S., Resnick, H.E., Carbone, L., Beamer, B.A,m Won Park, S., Lane, N.E., Harris,
T.B., and Cummings, S.R. Thiazolidinedione (TZD) use and change in bone density in older diabetic
adults. J Clin Endo Metab 91:3349-54, 2006.
• Lecka-Czernik, B., Suva, L. Resolving the two "bony" faces of PPAR-γ, PPAR Res 2006.
• Lecka-Czernik, B. Ackert-Bicknell, C.L., Adamo, M., Marmolejos, V., Churchill G.A., Shockley, K.R.,
Reid, I.R., Grey, A., Rosen, C.J. Activation of peroxisome proliferatoractivated receptor-gamma
(PPARgamma) by rosiglitazone suppresses components of the IGF regulatory system in vitro and in
vivo. Endocirnology 148:903-11, 2007.
• Lazarenko, O.P., Rzonca, S.O., Hogue, W.R., Swain, F.L., Suva, L.J., Lecka-Czernik, B. Rosiglitazone
induces decreases in bone mass and strength that are reminiscent of aged bone. Endocrinology
148:2669-80, 2007.
• Ackert-Bicknell, C.L., Skockley, K.R., Horton, L.G., Lecka-Czernik, B., Churchill, G.A., Rosen, C.J.
Strain specific effects of Rosiglitazone on bone mass, body composition and serum IGF-I. Endocrinology
150:1330-1340, 2009.
• Shockley, K.R., Lazarenko, O.P., Czernik, P.J., Rosen, C.J., Churchill, G.A., Lecka-Czernik, B. PPARg2
nuclear receptor controls multiple regulatory pathways of osteoblast differentiation from marrow
mesenchymal stem cell. J Cell Biochem 106:232-46, 2009.
• Lecka-Czernik, B. Bone is a target for type 2 diabetes treatment (review). Current Opinion in
Investigational Drugs (accepted).
• Huang, S., Kaw, M., Harris, M.T., Ebraheim, N., McInerney, M.F., Najjar, S.M., Lecka-Czernik, B.
Decreased Osteoclastogenesis and High Bone Mass in Mice with Impaired Insulin Clearance Due to
Liver-Specific Inactivation to CEACAM1. Bone (submitted)