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Originally published In Press as doi:10.1074/jbc.M103740200 on May 29, 2001

J. Biol. Chem., Vol. 276, Issue 31, 29307-29312, August 3, 2001
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Age-associated Differences in Cardiovascular Inflammatory Gene Induction during Endotoxic Stress*

Hiroshi Saito and John PapaconstantinouDagger

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 alpha  or inducible nitric-oxide synthase showed no age-associated differences, the induction of interleukin-1beta (IL-1beta ) 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.

Dagger 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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Copyright © 2001 by the American Society for Biochemistry and Molecular Biology.