A pertussis toxin sensitive G-protein-independent pathway is involved in serum amyloid A-induced formyl peptide receptor 2-mediated CCL2 production

Title
A pertussis toxin sensitive G-protein-independent pathway is involved in serum amyloid A-induced formyl peptide receptor 2-mediated CCL2 production
Author(s)
백석환이하영[이하영]김상두[김상두]심재웅[심재웅]김학정[김학정]윤진호[윤진호]김권회[김권회]배외식[배외식]
Keywords
ACUTE-PHASE PROTEIN; NF-KAPPA-B; HUMAN MONOCYTES; ENDOTHELIAL-CELLS; HUMAN NEUTROPHILS; COUPLED RECEPTOR; EXPRESSION; BINDING; ACTIVATION
Issue Date
201004
Publisher
KOREAN SOC MED BIOCHEMISTRY MOLECULAR BIOLOGY
Citation
EXPERIMENTAL AND MOLECULAR MEDICINE, v.42, no.4, pp.302 - 309
Abstract
Serum amyloid A (SAA) induced CCL2 production via a pertussis toxin (PTX)-insensitive pathway in human umbilical vein endothelial cells (HUVECs). SAA induced the activation of three MAPKs (ERK, p38 MAPK, and JNK), which were completely inhibited by knock-down of formyl peptide receptor 2 (FPR2). Inhibition of p38 MAPK and JNK by their specific inhibitors (SB203580 and SP600125), or inhibition by a dominant negative mutant of p38 MAPK dramatically decreased SAA-induced CCL2 production. Inactivation of G, protein(s) by PTX inhibited the activation of SAA-induced ERK, but not p38 MAPK or JNK. The results indicate that SAA stimulates FPR2-mediated activation of p38 MAPK and JNK, which are independent of a PTX-sensitive G-protein and are essential for SAA-induced CCL2 production.
URI
http://hdl.handle.net/YU.REPOSITORY/22591http://dx.doi.org/10.3858/emm.2010.42.4.029
ISSN
1226-3613
Appears in Collections:
의과대학 > 생화학.분자생물학교실 > Articles
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