PMID- 16158333
OWN - NLM
STAT- MEDLINE
DCOM- 20051017
LR  - 20161124
IS  - 1023-3830 (Print)
IS  - 1023-3830 (Linking)
VI  - 54
IP  - 8
DP  - 2005 Aug
TI  - Polyinosinic acid induces TNF and NO production as well as NF-kappaB and AP-1 
      transcriptional activation in the monocytemacrophage cell line RAW 264.7.
PG  - 328-37
AB  - OBJECTIVE: This study evaluates the poly inosinic acid (poly I)-induced 
      activation in the murine monocytemacrophage cell line RAW 264.7, which led to an 
      inflammatory phenotype. MATERIAL: RAW 264.7, and WEHI 164 cell lines were used. 
      RESULTS: The activation process is characterized by the acquisition of a mature 
      macrophage morphology and the production of inflammatory mediators tumor necrosis 
      factor (TNF) and nitric oxide (NO). The activation by poly I has distinctive 
      features. Thus, poly I induced an increase in nuclear factor kappaB (NF-kappaB) 
      transcriptional activity due to a long-term degradation of inhibitory NF-kappaB 
      (IkappaB) beta while lipopolysaccharide (LPS) induced the degradation of both 
      IkappaBalpha and IkappaBbeta. Poly I also induced an increase in activator 
      protein 1 (AP-1) transcriptional activity, possibly due to the activation of the 
      mitogen activated protein kinases (MAPKs) ERK, Jun N terminal kinase (JNK) and 
      p38. Dextran sulphate (DS) efficiently inhibited the activation induced by poly I 
      including the production of the inflammatory mediators. Dextran sulphate also 
      inhibited AP-1 and NF-kappaB transcriptional activities in poly I-stimulated 
      cells. RAW 264.7 cells express macrophage scavenger receptor 1 (Msr1) type I and 
      Msr1 type II that are differently up-regulated upon treatment with poly I. 
      CONCLUSIONS: The results presented demonstrate that the well-known blocker of 
      scavenger receptors poly I activates macrophages to produce TNF and NO, 
      triggering specific signal transduction pathways.
FAU - Campa, V M
AU  - Campa VM
AD  - Instituto Universitario de Oncologia del Principado de Asturias and Departamento 
      de Bioquimica y Biologia Molecular, Universidad de Oviedo, 33071 Oviedo, Spain.
FAU - Iglesias, J M
AU  - Iglesias JM
FAU - Carcedo, M T
AU  - Carcedo MT
FAU - Rodriguez, R
AU  - Rodriguez R
FAU - Riera, J
AU  - Riera J
FAU - Ramos, S
AU  - Ramos S
FAU - Lazo, P S
AU  - Lazo PS
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Switzerland
TA  - Inflamm Res
JT  - Inflammation research : official journal of the European Histamine Research 
      Society ... [et al.]
JID - 9508160
RN  - 0 (Dextrans)
RN  - 0 (I kappa B beta protein)
RN  - 0 (I-kappa B Proteins)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (NF-kappa B)
RN  - 0 (Nfkbia protein, mouse)
RN  - 0 (Receptors, Immunologic)
RN  - 0 (Receptors, Scavenger)
RN  - 0 (Transcription Factor AP-1)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 139874-52-5 (NF-KappaB Inhibitor alpha)
RN  - 25249-22-3 (Poly I)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - 9042-14-2 (Dextran Sulfate)
RN  - EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases)
RN  - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
SB  - IM
MH  - Animals
MH  - Blotting, Western
MH  - Cell Line
MH  - Dextran Sulfate/pharmacology
MH  - Dextrans/pharmacology
MH  - I-kappa B Proteins/metabolism
MH  - Inflammation
MH  - JNK Mitogen-Activated Protein Kinases/metabolism
MH  - Lipopolysaccharides/chemistry
MH  - Macrophages/metabolism
MH  - Mice
MH  - NF-KappaB Inhibitor alpha
MH  - NF-kappa B/*metabolism
MH  - Nitric Oxide/*metabolism
MH  - Poly I/*pharmacology
MH  - Receptors, Immunologic/metabolism
MH  - Receptors, Scavenger
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Signal Transduction
MH  - Time Factors
MH  - Transcription Factor AP-1/*metabolism
MH  - Transcription, Genetic
MH  - *Transcriptional Activation
MH  - Transfection
MH  - Tumor Necrosis Factor-alpha/*biosynthesis
MH  - Up-Regulation
MH  - p38 Mitogen-Activated Protein Kinases/metabolism
EDAT- 2005/09/15 09:00
MHDA- 2005/10/18 09:00
CRDT- 2005/09/15 09:00
PHST- 2005/09/15 09:00 [pubmed]
PHST- 2005/10/18 09:00 [medline]
PHST- 2005/09/15 09:00 [entrez]
AID - 10.1007/s00011-005-1359-4 [doi]
PST - ppublish
SO  - Inflamm Res. 2005 Aug;54(8):328-37. doi: 10.1007/s00011-005-1359-4.