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J. Biol. Chem., Vol. 276, Issue 31, 29307-29312, August 3, 2001
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From the Department of Human Biological Chemistry and Genetics,
University of Texas Medical Branch, Galveston,
Texas 77555-0643
Upon physiological stress, families of stress
response genes are activated as natural defense mechanisms. Here, we
show that induction of specific inflammatory genes is significantly
dysregulated and altered in the heart of aged (24-26-month-old)
versus young (4-month-old) mice experimentally challenged
with a bacterial endotoxin, lipopolysaccharide (LPS, 1.5 mg/kg of body
mass). Whereas the LPS-mediated induction of cardiac mRNA
for tumor necrosis factor
Age-associated Differences in Cardiovascular
Inflammatory Gene Induction during Endotoxic Stress*
or inducible nitric-oxide synthase
showed no age-associated differences, the induction of interleukin-1
(IL-1) and intracellular adhesion molecule-1 was modestly extended
with aging, and the induction of IL-6 was significantly prolonged with
aging. This age-associated phenomenon occurred gradually from 4 to 17 months of age and became more evident after 23 months of age. The
age-associated augmentation of the cardiac IL-6 induction was also
dramatic at the protein level. Immunohistochemically, the LPS-induced
cardiac IL-6 was localized mainly in the microvascular walls. Aged but not young mice showed a high mortality rate during these experiments. These results demonstrate that endotoxin-mediated induction of specific
inflammatory genes in cardiovascular tissues is altered with aging,
which may be causally related to the increased susceptibility of aged
animals to endotoxic stress.
*
This work was supported by Grant-in-aid 97G-654 from the
American Heart Association, Texas Affiliate, a Seed Money grant from the University of Texas Medical Branch Sealy Center on Aging (to H. S.), and Grant 2-P01-AG10514 from the NIA, National Institutes of
Health (to J. P.; publication number 114).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed: Dept. of Human
Biological Chemistry and Genetics, University of Texas Medical Branch,
301 University Boulevard, Galveston, TX 77555-0643. Tel.: 409-772-2761; Fax: 409-772-9216; E-mail: jpapacon@utmb.edu.
Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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