PMID- 16755143
OWN - NLM
STAT- MEDLINE
DCOM- 20060707
LR  - 20091119
IS  - 0916-9636 (Print)
IS  - 0916-9636 (Linking)
VI  - 29
IP  - 2
DP  - 2006 Feb
TI  - Increased migration of vascular adventitial fibroblasts from spontaneously 
      hypertensive rats.
PG  - 95-103
AB  - Experimental evidence has suggested that vascular adventitial fibroblasts (AFs) 
      may migrate into the neointima of arteries after balloon injury in various animal 
      models. However, the research on migration of AFs has been limited to the effects 
      of acute vascular injury. The role of AFs in chronic vascular injury and 
      hypertension is not yet known. In this study, the migration of spontaneously 
      hypertensive rat (SHR)-AFs and Wistar-Kyoto rat (WKY)-AFs from the thoracic aorta 
      was determined by a transwell technique. Our results showed that fetal calf 
      serum, angiotensin II (Ang II), phorbol ester, basic fibroblast growth factor and 
      platelet-derived growth factor-BB induced migration in a dose-dependent manner, 
      and the migration of SHR-AFs was always greater than that of WKY-AFs. Ang 
      II-induced migration of AFs was considered to have been mediated by Ang II type 1 
      receptor (AT1-R), because the AT1-R antagonist losartan (10(-7)-10(-5) mol/l) 
      suppressed Ang II-induced migration. Ang II-induced migration was also blocked by 
      the extracellular-regulated protein kinase 1/2 (ERK1/2) inhibitor PD98059 (10(-5) 
      mol/l) and p38 kinase inhibitor SB202190 (10(-5) mol/l), indicating that ERK1/2 
      and p38 kinase were involved in Ang II-induced migration. Ang II (10(-7) 
      mol/l)-induced ERK1/2 and p38 kinase phosphorylation, both of which peaked after 
      5 min, were suppressed by PD98059 and SB202190, respectively. The Ang-II induced 
      phosphorylation of both proteins was suppressed by losartan, whereas no effect 
      was observed with PD123319, a specific inhibitor of Ang II type 2 receptor 
      (AT2-R). Thus, in the present study, various factors stimulated the migration of 
      SHR-AFs and, to a leber extent, WKY-AFs from the thoracic aorta, and the ERK1/2 
      and p38 kinase pathways are involved in Ang II-stimulated migration of 
      fibroblasts.
FAU - Li, Li
AU  - Li L
AD  - Shanghai Key Laboratory of Vascular Biology, Ruijin Hospital and Institute of 
      Health Sciences, Shanghai, PR China.
FAU - Zhu, Ding-Liang
AU  - Zhu DL
FAU - Shen, Wei-Li
AU  - Shen WL
FAU - Gao, Ping-Jin
AU  - Gao PJ
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Hypertens Res
JT  - Hypertension research : official journal of the Japanese Society of Hypertension
JID - 9307690
RN  - 11128-99-7 (Angiotensin II)
RN  - EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
RN  - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
SB  - IM
MH  - Angiotensin II/metabolism/physiology
MH  - Animals
MH  - Aorta, Thoracic/cytology
MH  - Cell Movement/*physiology
MH  - Cells, Cultured
MH  - Extracellular Signal-Regulated MAP Kinases/metabolism
MH  - Fibroblasts/*physiology
MH  - Hypertension/metabolism/*physiopathology
MH  - MAP Kinase Signaling System
MH  - Male
MH  - Phosphorylation
MH  - Rats
MH  - Rats, Inbred SHR
MH  - Rats, Inbred WKY
MH  - Signal Transduction
MH  - p38 Mitogen-Activated Protein Kinases/metabolism
EDAT- 2006/06/07 09:00
MHDA- 2006/07/11 09:00
CRDT- 2006/06/07 09:00
PHST- 2006/06/07 09:00 [pubmed]
PHST- 2006/07/11 09:00 [medline]
PHST- 2006/06/07 09:00 [entrez]
AID - JST.JSTAGE/hypres/29.95 [pii]
AID - 10.1291/hypres.29.95 [doi]
PST - ppublish
SO  - Hypertens Res. 2006 Feb;29(2):95-103. doi: 10.1291/hypres.29.95.