| Literature DB >> 30044978 |
Georgios K Paschos1, Soon Yew Tang1, Katherine N Theken1, Xuanwen Li1, Ioannis Verginadis2, Damien Lekkas1, Lindsay Herman1, Weili Yan1, John Lawson1, Garret A FitzGerald3.
Abstract
Previous studies using genetic mouse models have implicated COX-2 in the browning of white adipose tissues (WATs) in mice during cold exposure. However, COX-2 is important during development, and conventional knockouts (KOs) exhibit many defects, conditioned by genetic background. Similarly, the physiological relevance of transgenic overexpression of COX-2 is questionable. In the present study, we utilized mice in which COX-2 was deleted postnatally, bypassing the consequences of enzyme deficiency during development. Despite activation of thermogenesis and browning of inguinal WAT, cold exposure failed to increase COX-2 expression in the adipose tissues of mice with different genetic backgrounds, and the body temperature response to cold was unaltered in postnatal global COX-2 KOs. Selective disruption of COX-2 in adipose tissues also failed detectably to impact systemic prostaglandin biosynthesis. Browning of inguinal WATs induced by exposure to cold is independent of adipose tissue COX-2.Entities:
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Year: 2018 PMID： 30044978 PMCID： PMC6118132 DOI： 10.1016/j.celrep.2018.06.082
Source DB: PubMed Journal: Cell Rep Impact factor: 9.423