Absence of Myeloid COX-2 Attenuates Acute Inflammation but Does Not Influence Development of Atherosclerosis in Apolipoprotein E Null Mice

作者：Narasimha Ajay J; Watanabe Junji; Ishikawa Tomo o; Priceman Saul J; Wu Lily; Herschman Harvey R; Reddy Srinivasa T^*

来源：Arteriosclerosis, Thrombosis, and Vascular Biology, 2010, 30(2): 260-U254.

DOI：10.1161/ATVBAHA.109.198762

• atherosclerosis
• cyclooxygenase-2
• inflammation
• myeloid cells
• prostanoids

Objective-The role of myeloid cell cyclooxygenase-2 (COX-2) in the progression of atherosclerosis has not been clearly defined.
Methods and Results-We investigated the role of COX-2 expressed in the myeloid lineage in the development of atherosclerosis using a myeloid-specific COX-2(-/-) (COX-2(-M/-M)) mouse on a hyperlipidemic apolipoprotein (apo) E(-/-) background (COX-2(-M/-M)/apoE(-/-)). Myeloid COX-2 depletion resulted in significant attenuation of acute inflammation corresponding with decreased PGE2 levels in an air pouch model. COX-2 depletion in myeloid cells did not influence development of atherosclerosis in COX-2(-M/-M)/apoE(-/-) when compared to apoE(-/-) littermates fed either chow or western diets. The unanticipated lack of contribution of myeloid COX-2 to the development atherosclerosis is not attributable to altered maintenance, differentiation, or mobilization of myeloid and lymphoid populations. Moreover, myeloid COX-2 depletion resulted in unaltered serum prostanoid levels and cellular composition of atherosclerotic lesions of COX-2(-M/-M)/apoE(-/-) mice.
Conclusions-Our results suggest that COX-2 expression in myeloid cells, including macrophages, does not influence the development of atherosclerosis in mice. (Arterioscler Thromb Vasc Biol. 2010; 30:260-268.)

• 出版日期2010-2