title: The effect of the expression of angiotensin II on extracellular matrix metalloproteinase inducer (EMMPRIN) in macrophages is mediated via the AT1/COX-2/PGE2 pathway.
abstract: OBJECTIVE
  To explore the expression of extracellular matrix metalloproteinase inducer (EMMPRIN) in THP-1 macrophages induced by angiotensin II (Ang II) and the mechanism of EMMPRIN expression.
  
  
  METHODS
  THP-1 cells were cultured and induced into macrophages, then stimulated with 10(-6) mol/L Ang II. Levels of EMMPRIN gene and its protein were measured by real-time polymerase chain reaction and western blotting. Prostaglandin E(2) (PGE(2)) expression was assayed by enzyme-linked immunosorbent assay. Antagonists of the angiotensin type-1 receptor (AT(1)R) and angiotensin type-2 receptor (AT(2)R) were used to inhibit the effect of Ang II, and PGE(2) added to detail the mechanism of Ang II-induced EMMPRIN expression.
  
  
  RESULTS
  Ang II clearly induced the expression of EMMPRIN mRNA and protein in macrophages; this expression peaked at 12 h and declined after 24 h. The tendency of enhancement of the levels of cyclooxygenase-2 (COX-2) and PGE(2) was coincident with EMMPRIN expression. AT(1)-receptor antagonists and COX-2 inhibitors inhibited the effect of Ang II, but AT(2)-receptor antagonists did not.
  
  
  CONCLUSIONS
  Ang II can up-regulate EMMPRIN expression in THP-1 macrophages via the AT(1)/COX-2/PGE(2) signal transduction pathway, and the effect can be inhibited by losartan and NS-398.
authors.affiliation: Department of Cardiology, Kunming General Hospital of Chengdu Military Area, Yunnan, 650032, China. doctorlxyang@163.com
authors.forename: Li-xia
authors.initials: LX
authors.lastname: Yang
authors.forename: Jin-shan
authors.initials: JS
authors.lastname: Ye
authors.forename: Rui-wei
authors.initials: RW
authors.lastname: Guo
authors.forename: Hong
authors.initials: H
authors.lastname: Liu
authors.forename: Xian-mei
authors.initials: XM
authors.lastname: Wang
authors.forename: Feng
authors.initials: F
authors.lastname: Qi
authors.forename: Chuanming
authors.initials: C
authors.lastname: Guo
mesh_terms: D000804:Angiotensin II / Q000378:metabolism*; D047228:Angiotensin II Type 1 Receptor Blockers / Q000494:pharmacology; D057912:Angiotensin II Type 2 Receptor Blockers / Q000494:pharmacology; D000818:Animals; D051926:Basigin; D002460:Cell Line; D051546:Cyclooxygenase 2 / Q000378:metabolism*; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D015232:Dinoprostone / Q000378:metabolism*; D006801:Humans; D007093:Imidazoles / Q000494:pharmacology; D019808:Losartan / Q000494:pharmacology; D008264:Macrophages / Q000166:cytology / Q000378:metabolism*; D009578:Nitrobenzenes / Q000494:pharmacology; D011725:Pyridines / Q000494:pharmacology; D044140:Receptor, Angiotensin, Type 1 / Q000378:metabolism*; D015398:Signal Transduction / Q000187:drug effects / Q000502:physiology*; D013449:Sulfonamides / Q000494:pharmacology
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D057912:Angiotensin II Type 2 Receptor Blockers; D016861:Cyclooxygenase Inhibitors; D007093:Imidazoles; D009578:Nitrobenzenes; D011725:Pyridines; D044140:Receptor, Angiotensin, Type 1; D013449:Sulfonamides; D000804:Angiotensin II; C080955:N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide; C073402:PD 123319; D051926:Basigin; D051546:Cyclooxygenase 2; D019808:Losartan; D015232:Dinoprostone