PMID- 9351439
OWN - NLM
STAT- MEDLINE
DCOM- 19971202
LR  - 20190706
IS  - 0009-7330 (Print)
IS  - 0009-7330 (Linking)
VI  - 81
IP  - 5
DP  - 1997 Nov
TI  - Increased expression of interleukin-1 beta and monocyte chemotactic and 
      activating factor/monocyte chemoattractant protein-1 in the hypertrophied and 
      failing heart with pressure overload.
PG  - 664-71
AB  - Studies on the effects of proinflammatory cytokines on the heart suggest that 
      they play some roles in the pathogenesis of congestive heart failure (CHF). To 
      determine the involvement of proinflammatory cytokine in cardiac hypertrophy and 
      CHF induced by mechanical overload, we investigated the expression of interleukin 
      (IL)-1 beta and monocyte chemotactic and activating factor (MCAF)/monocyte 
      chemoattractant protein-1 (MCP-1) in the left ventricle (LV) of Dahl 
      salt-sensitive (DS) rats that showed hypertrophy of the LV induced by 
      hypertension and subsequently developed CHF. The IL-1 beta mRNA content in the LV 
      of DS rats increased 3.9-fold when LV hypertrophy developed, and the increase 
      reached 6.2-fold at the CHF stage compared with that of age-matched Dahl 
      salt-resistant (DR) rats. The amount of IL-1 beta in the LV was positively 
      correlated with the LV weight/body weight ratio. Most of the IL-1 beta 
      immunoreactivity was localized in the endothelial cells and interstitial 
      macrophages. The mRNA levels of MCAF in the LV increased 3.6-fold at 11 weeks and 
      reached 4.8-fold at the CHF stage relative to the age-matched DR rats. MCAF 
      protein was localized to the endothelial cells and interstitial macrophages. In 
      DS rats, the number of interstitial macrophages increased diffusely throughout 
      the LV. We suggest that increased chemokine expression, macrophage infiltration, 
      and proinflammatory cytokine expression play some role in the pathogenesis of 
      cardiac hypertrophy and failure induced by chronic mechanical overload.
FAU - Shioi, T
AU  - Shioi T
AD  - Department of Cardiovascular Medicine, Kyoto University, Japan.
FAU - Matsumori, A
AU  - Matsumori A
FAU - Kihara, Y
AU  - Kihara Y
FAU - Inoko, M
AU  - Inoko M
FAU - Ono, K
AU  - Ono K
FAU - Iwanaga, Y
AU  - Iwanaga Y
FAU - Yamada, T
AU  - Yamada T
FAU - Iwasaki, A
AU  - Iwasaki A
FAU - Matsushima, K
AU  - Matsushima K
FAU - Sasayama, S
AU  - Sasayama S
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Circ Res
JT  - Circulation research
JID - 0047103
RN  - 0 (Chemokine CCL2)
RN  - 0 (Interleukin-1)
SB  - IM
MH  - Animals
MH  - *Blood Pressure
MH  - Cardiomegaly/*metabolism/physiopathology
MH  - Chemokine CCL2/*biosynthesis
MH  - Heart Failure/*metabolism/physiopathology
MH  - Immunohistochemistry
MH  - Interleukin-1/*biosynthesis
MH  - Male
MH  - Organ Size
MH  - Rats
EDAT- 1997/11/14 00:00
MHDA- 1997/11/14 00:01
CRDT- 1997/11/14 00:00
PHST- 1997/11/14 00:00 [pubmed]
PHST- 1997/11/14 00:01 [medline]
PHST- 1997/11/14 00:00 [entrez]
AID - 10.1161/01.res.81.5.664 [doi]
PST - ppublish
SO  - Circ Res. 1997 Nov;81(5):664-71. doi: 10.1161/01.res.81.5.664.