Dr. Aksam J. Merched's Lab
 | |  | |  | |  |
Assistant Professor,
Department of Molecular & Cellular Biology
Ph.D., University of Nancy, France
Postdoctoral, Baylor College of Medicine
Lau PP, Li L, Merched AJ, Zhang AL, Ko KWS and
Chan L. (2006). Nicotine Induces Proinflammatory
Responses in Macrophages and the Aorta
Leading to Acceleration of Atherosclerosis in
LDLR-/- Mice. Arteriosclerosis Thrombosis and
Vascular Biology. 26(1):143-149
Merched A and Chan L. (2004). Absence of
p21(Waf1/Cip1/Sdi1) Modulates Macrophage
Differentiation and Inflammatory Response and
Protects Against Atherosclerosis. Circulation.
110(25):3830-3841.
Nomura S, Merched A, Nour E, Dieker C, Oka K
and Chan L. (2004). LDL Receptor gene therapy
with helper-dependent adenovirus produces
long-term protection in a mouse model of familial
hypercholesterolemia. Gene Therapy.
11(20):1540-1548.
Serhan CN, Jain A, Marleau S, Clish C, Kantarci A,
Behbehani B, Colgan SP, Stahl GL, Merched A,
Petasis NA, Chan L, and Van Dyke TE. (2003).
Reduced inflammation and tissue damage in
transgenic rabbits overexpressiong
15-lipoxygenase and endogenous
anti-inflammatory lipid mediators. Journal of
Immunology. 171: 6856-6865.
Merched A, Williams L and Chan L. (2003).
Macrophage-specific p53 expression plays a
crucial role in atherosclerosis development and
plaque remodeling. Arteriosclerosis Thrombosis
and Vascular Biology. 23(9):1608-14..
Belalcazar M*, Merched A*, Carr B, Oka K, Chen
K-H, Pastore L, Beaudet A, Chan L. (2003).
Long-term stable expression of human
apolipoprotein A-I mediated by helper-dependent
adenovirus gene transfer inhibits atherosclerosis
progression and remodels atherosclerotic
plaques in a mouse model of familial
hypercholesterolemia (* equal contribution).
Circulation 107:2726-2732.
Oka K, Pastore L, Kim I-H, Merched A, Nomura S,
Lee HJ, Merched-Sauvage M, Arden-Riley C, Lee B,
Finegold M, Beaudet A, Chan L .(2001). Long-term
reversal of hypercholesterolemia and prevention of
atherosclerosis development in LDL
receptor-deficient mice by transfer of the VLDL
receptor gene in vivo using helper-dependent
adenoviral vector. Circulation. 103(9):1274-1281.
research of cardiovascular diseases and atherosclerosis or
hardening of the arteries.
A large part of Dr. Merched’s current research effort consist of
understanding genes contributing to the build up of
atherosclerotic lesions. All stages of the pathological process
are investigated including recruitment of inflammatory cells to
sites of injury in the arterial wall, lipid uptake and accumulation,
cell death and proliferation. Success depends on keeping up
with the latest cellular and molecular technical advances,
surgical procedures, using and creating the latest genetically
modified animal models.
His awards and honors include American Heart Association,
French Ministry of Education, Bayer Pharmaceuticals, French
Committee for Coordination of Research in Atherosclerosis
and Cholesterol and Lipids, Hariri Foundation.
Dr. Merched has authored and co-authored over 45
publications, invited talks, and conference proceedings. He is
currently a member of the American Heart Association, the
International Society of Atherosclerosis, and the American
Society of Gene Therapy.
The practical objective of our research is to understand the
genetic information and the regulation pathways to identify
pharmaceutical targets and to design more efficacious
interventions. Our studies are defining, at the molecular level,
novel mechanisms of atherogenesis.
(c)1998-2006 Baylor College of Medicine
Aksam J. Merched, Ph.D.
Department of Molecular and Cellular Biology
One Baylor Plaza, Houston, TX 77030
Mail: One Baylor Plaza, Mail Stop BCM603, Houston, TX 77030
Phone: 713-798-4999 | Fax: 713-798-8764
E-mail: amerched@bcm.edu
Last Modified: April 30, 2006