PMID- 15087417
OWN - NLM
STAT- MEDLINE
DCOM- 20041015
LR  - 20141120
IS  - 1524-4571 (Electronic)
IS  - 0009-7330 (Linking)
VI  - 94
IP  - 10
DP  - 2004 May 28
TI  - Bradykinin B1 receptor expression induced by tissue damage in the rat portal 
      vein: a critical role for mitogen-activated protein kinase and nuclear 
      factor-kappaB signaling pathways.
PG  - 1375-82
AB  - The bradykinin B1 receptor (B1R) is normally absent under physiological 
      conditions, but is highly inducible during inflammatory conditions or following 
      tissue damage. The present study attempted to determine some of the mechanisms 
      underlying B1R upregulation following tissue injury in rat portal vein. Damage 
      induced by tissue isolation and in vitro incubation caused a significant and 
      time-dependent increase in des-Arg9-bradykinin (des-Arg9-BK) responsiveness that 
      paralleled the B1R mRNA expression, as confirmed by real-time quantitative PCR. 
      In vitro incubation of rat portal vein also induced the activation of some 
      members of the mitogen activated protein kinase (MAPK) family, namely, 
      extracellular signal-regulated kinase (ERK), c-Jun NH2-terminal kinase (JNK), and 
      p38 MAPK, an effect accompanied by degradation of the inhibitory protein 
      IkappaBalpha and translocation of nuclear transcription factor-kappaB (NF-kappaB) 
      to the nucleus. The blockade of p38 MAPK, JNK or NF-kappaB, but not ERK pathways 
      with selective inhibitors, resulted in a significant reduction of the upregulated 
      contractile response caused by the selective B1R agonist des-Arg9-BK, and largely 
      prevented the induction of B1R mRNA expression in the rat portal vein. Together, 
      these results demonstrate that in vitro tissue damage induces activation of 
      several intracellular signaling pathways that have a key role in the control of 
      B1R expression. B1R could exert a pivotal role in the development of the 
      cardiovascular response associated with vascular damage.
FAU - Medeiros, Rodrigo
AU  - Medeiros R
AD  - Department of Pharmacology, Universidade Federal de Santa Catarina, Brazil.
FAU - Cabrini, Daniela A
AU  - Cabrini DA
FAU - Ferreira, Juliano
AU  - Ferreira J
FAU - Fernandes, Elizabeth S
AU  - Fernandes ES
FAU - Mori, Marcelo A S
AU  - Mori MA
FAU - Pesquero, Joao B
AU  - Pesquero JB
FAU - Bader, Michael
AU  - Bader M
FAU - Avellar, Maria C W
AU  - Avellar MC
FAU - Campos, Maria M
AU  - Campos MM
FAU - Calixto, Joao B
AU  - Calixto JB
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20040415
PL  - United States
TA  - Circ Res
JT  - Circulation research
JID - 0047103
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (NF-kappa B)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptor, Bradykinin B1)
RN  - 15958-92-6 (bradykinin, des-Arg(9)-)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
RN  - S8TIM42R2W (Bradykinin)
SB  - IM
MH  - Animals
MH  - Bradykinin/*analogs & derivatives/pharmacology
MH  - Enzyme Inhibitors/pharmacology
MH  - Gene Expression Regulation
MH  - In Vitro Techniques
MH  - MAP Kinase Signaling System
MH  - Mitogen-Activated Protein Kinases/antagonists & inhibitors/metabolism/*physiology
MH  - NF-kappa B/antagonists & inhibitors/metabolism/*physiology
MH  - Portal Vein/anatomy & histology/enzymology/*metabolism
MH  - RNA, Messenger/metabolism
MH  - Rats
MH  - Receptor, Bradykinin B1/*biosynthesis/genetics
MH  - Signal Transduction
MH  - Up-Regulation
EDAT- 2004/04/17 05:00
MHDA- 2004/10/16 09:00
CRDT- 2004/04/17 05:00
PHST- 2004/04/17 05:00 [pubmed]
PHST- 2004/10/16 09:00 [medline]
PHST- 2004/04/17 05:00 [entrez]
AID - 01.RES.0000128404.65887.08 [pii]
AID - 10.1161/01.RES.0000128404.65887.08 [doi]
PST - ppublish
SO  - Circ Res. 2004 May 28;94(10):1375-82. doi: 10.1161/01.RES.0000128404.65887.08. 
      Epub 2004 Apr 15.