PMID- 15051638
OWN - NLM
STAT- MEDLINE
DCOM- 20040819
LR  - 20220331
IS  - 1524-4539 (Electronic)
IS  - 0009-7322 (Linking)
VI  - 109
IP  - 14
DP  - 2004 Apr 13
TI  - Thermal treatment attenuates neointimal thickening with enhanced expression of 
      heat-shock protein 72 and suppression of oxidative stress.
PG  - 1763-8
AB  - BACKGROUND: The beneficial effects of thermal therapy have been reported in 
      several cardiovascular diseases. However, it is unknown whether the thermal 
      treatment has some beneficial roles against the development of atherosclerosis. 
      METHODS AND RESULTS: The inflammatory arterial lesion was introduced by placement 
      of a polyethylene cuff on femoral arteries of male Sprague-Dawley rats for 4 
      weeks. Thermal-treated group underwent daily bathing in 41 degrees C hot water 
      for 15 minutes. Neointimal thickening along with immunohistochemical expression 
      of heat-shock proteins (HSPs), monocyte chemoattractant protein-1 (MCP-1), and 
      NADPH oxidase were compared with those of a thermally untreated (Control) group. 
      Morphometric analysis demonstrated a significant suppression of neointimal 
      thickening in thermal-treated group compared with the Control group 
      (intimal/medial area ratios, 0.01+/-0.01 versus 0.31+/-0.04, P<0.01). Expression 
      of MCP-1 and infiltration of ED-positive cells were enhanced in the adventitial 
      layer of Control. More importantly, expression of HSP72 in media was enhanced by 
      thermal treatment. Expression of p22-phox, the major membrane subunit of NADPH 
      oxidase, and MCP-1 was augmented in cuff-injured adventitia of the Control but 
      not the thermal-treated groups. CONCLUSIONS: Thermal treatment significantly 
      attenuated infiltration of inflammatory cells in adventitia and suppressed 
      neointimal thickening in cuff-injured arteries with the enhancement of HSP72 
      expression and suppression of oxidative stress.
FAU - Okada, Motoi
AU  - Okada M
AD  - First Department of Medicine, Asahikawa Medical College, Asahikawa, Japan.
FAU - Hasebe, Naoyuki
AU  - Hasebe N
FAU - Aizawa, Yoshiaki
AU  - Aizawa Y
FAU - Izawa, Kazuma
AU  - Izawa K
FAU - Kawabe, Jun-ichi
AU  - Kawabe J
FAU - Kikuchi, Kenjiro
AU  - Kikuchi K
LA  - eng
PT  - Evaluation Study
PT  - Journal Article
DEP - 20040329
PL  - United States
TA  - Circulation
JT  - Circulation
JID - 0147763
RN  - 0 (Ccl2 protein, rat)
RN  - 0 (Chemokine CCL2)
RN  - 0 (HSP72 Heat-Shock Proteins)
RN  - 0 (Heat-Shock Proteins)
RN  - 0 (Membrane Transport Proteins)
RN  - 0 (Phosphoproteins)
RN  - 0 (Reactive Oxygen Species)
RN  - EC 1.6.3.- (NADPH Oxidases)
RN  - EC 1.6.3.1 (CYBA protein, human)
RN  - EC 1.6.99.1 (NADPH Dehydrogenase)
SB  - IM
MH  - Animals
MH  - Aorta, Thoracic
MH  - Arteriosclerosis/pathology/*prevention & control
MH  - *Baths
MH  - Chemokine CCL2/biosynthesis/genetics
MH  - Disease Models, Animal
MH  - Femoral Artery/injuries/*pathology
MH  - Fibroblasts/metabolism
MH  - Gene Expression Regulation
MH  - HSP72 Heat-Shock Proteins
MH  - Heat-Shock Proteins/*biosynthesis/genetics/physiology
MH  - Hot Temperature
MH  - *Hyperthermia, Induced
MH  - Hypertrophy
MH  - Implants, Experimental/adverse effects
MH  - Male
MH  - Membrane Transport Proteins/biosynthesis/genetics
MH  - NADPH Dehydrogenase/biosynthesis/genetics
MH  - NADPH Oxidases
MH  - Oxidative Stress
MH  - Phosphoproteins/biosynthesis/genetics
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Reactive Oxygen Species
MH  - Tunica Intima/*ultrastructure
MH  - Vasculitis/pathology/prevention & control
EDAT- 2004/03/31 05:00
MHDA- 2004/08/20 05:00
CRDT- 2004/03/31 05:00
PHST- 2004/03/31 05:00 [pubmed]
PHST- 2004/08/20 05:00 [medline]
PHST- 2004/03/31 05:00 [entrez]
AID - 01.CIR.0000124226.88860.55 [pii]
AID - 10.1161/01.CIR.0000124226.88860.55 [doi]
PST - ppublish
SO  - Circulation. 2004 Apr 13;109(14):1763-8. doi: 10.1161/01.CIR.0000124226.88860.55. 
      Epub 2004 Mar 29.