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Aging (Albany NY). 2016 Oct 7;8(10):2392-2406. doi: 10.18632/aging.101060.

Transgenic expression of cyclooxygenase-2 (COX2) causes premature aging phenotypes in mice.

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Department of Biological Sciences, University of South Carolina, Columbia, SC 29208, USA.
Center for Colon Cancer Research, University of South Carolina, Columbia, SC 29208, USA.
Department of Pathology, Microbiology & Immunology, School of Medicine, University of South Carolina, Columbia, SC 29209, USA.


Cyclooxygenase (COX) is a key enzyme in the biosynthesis of prostanoids, lipid signaling molecules that regulate various physiological processes. COX2, one of the isoforms of COX, is highly inducible in response to a wide variety of cellular and environmental stresses. Increased COX2 expression is thought to play a role in the pathogenesis of many age-related diseases. COX2 expression is also reported to be increased in the tissues of aged humans and mice, which suggests the involvement of COX2 in the aging process. However, it is not clear whether the increased COX2 expression is causal to or a result of aging. We have now addressed this question by creating an inducible COX2 transgenic mouse model. Here we show that post-natal expression of COX2 led to a panel of aging-related phenotypes. The expression of p16, p53, and phospho-H2AX was increased in the tissues of COX2 transgenic mice. Additionally, adult mouse lung fibroblasts from COX2 transgenic mice exhibited increased expression of the senescence-associated β-galactosidase. Our study reveals that the increased COX2 expression has an impact on the aging process and suggests that modulation of COX2 and its downstream signaling may be an approach for intervention of age-related disorders.


COX2; TP53; p16; premature aging; prostaglandin

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