PMID- 15253109
OWN - NLM
STAT- MEDLINE
DCOM- 20040914
LR  - 20191026
IS  - 0916-9636 (Print)
IS  - 0916-9636 (Linking)
VI  - 27
IP  - 6
DP  - 2004 Jun
TI  - Dual effects of endothelin-1 (1-31): induction of mesangial cell migration and 
      facilitation of monocyte recruitment through monocyte chemoattractant protein-1 
      production by mesangial cells.
PG  - 433-40
AB  - We previously found that human chymase selectively cleaves big endothelin-1 
      (ET-1) at the Tyr31-Gly32 bond and produces 31-amino acid endothelins, ET-1 
      (1-31), without any further degradation products. In this study, we investigated 
      the effect of ET-1 (1-31) on the migration of cultured rat mesangial cells (RMCs) 
      and on cells of the human monocytic cell line, THP-1. In addition, we examined 
      the interaction between RMCs and THP-1 cells using conditioned media from ET-1 
      (1-31)-stimulated RMCs. ET-1 (1-31) caused an increase in RMC migration in a 
      concentration-dependent manner, and the degree of increase was similar to those 
      by ET-1 and angiotensin II (All). The ET-1 (1-31)-induced increase in RMC 
      migration was inhibited by BQ123, an endothelin ETA receptor antagonist, but not 
      by BQ788, an endothelin ETB receptor antagonist. ET-1 (1-31) alone did not cause 
      significant migration of THP-1 cells. However, significant recruitment of THP-1 
      cells was observed with conditioned media taken from ET-1 (1-31)-stimulated RMCs. 
      The conditioned media-induced migration of THP-1 cells was inhibited by BQ123, 
      but not by BQ788. Western blotting analysis of the lysate of RMCs revealed that 
      the expression of monocyte chemoattractant protein-1 (MCP-1) protein in RMCs was 
      increased by treatment with ET-1 (1-31). The addition of neutralizing antibody 
      for MCP-1 to the medium inhibited the migration of THP-1 cells induced by 
      conditioned media from ET-1 (1-31)-stimulated RMCs. These findings suggest that 
      ET-1 (1-31) play a role in glomerulonephritis (GN) via dual effects that directly 
      cause the migration of mesangial cells (MCs) and may be responsible for the 
      recruitment of mononuclear cells mediated through the activation of MCs. Since 
      human chymase has been reported to be involved in glomerular disease, ET-1 (1-31) 
      may be among the mediators.
FAU - Ishizawa, Keisuke
AU  - Ishizawa K
AD  - Department of Pharmacology, University of Tokushima School of Medicine, Japan.
FAU - Yoshizumi, Masanori
AU  - Yoshizumi M
FAU - Tsuchiya, Koichiro
AU  - Tsuchiya K
FAU - Houchi, Hitoshi
AU  - Houchi H
FAU - Minakuchi, Kazuo
AU  - Minakuchi K
FAU - Izawa, Yuki
AU  - Izawa Y
FAU - Kanematsu, Yasuhisa
AU  - Kanematsu Y
FAU - Kagami, Shoji
AU  - Kagami S
FAU - Hirose, Masao
AU  - Hirose M
FAU - Tamaki, Toshiaki
AU  - Tamaki T
LA  - eng
PT  - Journal Article
PL  - England
TA  - Hypertens Res
JT  - Hypertension research : official journal of the Japanese Society of Hypertension
JID - 9307690
RN  - 0 (Antibodies)
RN  - 0 (Antihypertensive Agents)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Culture Media, Conditioned)
RN  - 0 (Endothelin-1)
RN  - 0 (Peptide Fragments)
RN  - 0 (Peptides, Cyclic)
RN  - 0 (endothelin-1 (1-31))
RN  - S2A8YZM151 (cyclo(Trp-Asp-Pro-Val-Leu))
SB  - IM
MH  - Animals
MH  - Antibodies/pharmacology
MH  - Antihypertensive Agents/pharmacology
MH  - Cell Movement/*drug effects
MH  - Cells, Cultured
MH  - Chemokine CCL2/immunology/*metabolism
MH  - Culture Media, Conditioned/pharmacology
MH  - Endothelin-1/*analogs & derivatives/*pharmacology
MH  - Glomerular Mesangium/*cytology/*drug effects/metabolism
MH  - Peptide Fragments/*pharmacology
MH  - Peptides, Cyclic/pharmacology
MH  - Rats
MH  - Rats, Sprague-Dawley
EDAT- 2004/07/16 05:00
MHDA- 2004/09/15 05:00
CRDT- 2004/07/16 05:00
PHST- 2004/07/16 05:00 [pubmed]
PHST- 2004/09/15 05:00 [medline]
PHST- 2004/07/16 05:00 [entrez]
AID - 10.1291/hypres.27.433 [doi]
PST - ppublish
SO  - Hypertens Res. 2004 Jun;27(6):433-40. doi: 10.1291/hypres.27.433.