Tang, Eva H C <br/><br/>
Deletion of EP4 on bone marrow-derived cells enhances inflammation and angiotensin II-induced abdominal aortic aneurysm formation.  [electronic resource] 

 -  Arteriosclerosis, thrombosis, and vascular biology  Feb 2011 
 - 261-9 p.  digital 
<br/><br/> Publication Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't 
<br/><br/><label>ISSN: </label>1524-4636 
<br/><br/><label>Standard No.: </label>10.1161/ATVBAHA.110.216580  doi 
<br/><br/><label>Subjects--Topical Terms: </label><br/>Angiotensin II--adverse effects<br/>Animals<br/>Aortic Aneurysm, Abdominal--chemically induced<br/>Bone Marrow Cells--cytology<br/>Bone Marrow Transplantation<br/>Chemokine CCL2--metabolism<br/>Elastin--metabolism<br/>Female<br/>Gene Deletion<br/>Hyperlipidemias--complications<br/>Inflammation--chemically induced<br/>Male<br/>Mice<br/>Mice, Inbred C57BL<br/>Mice, Knockout<br/>Models, Animal<br/>Receptors, LDL--genetics<br/>Receptors, Prostaglandin E, EP4 Subtype--genetics<br/>Risk Factors