PMID- 12950323
OWN - NLM
STAT- MEDLINE
DCOM- 20040421
LR  - 20220409
IS  - 1475-0961 (Print)
IS  - 1475-0961 (Linking)
VI  - 23
IP  - 5
DP  - 2003 Sep
TI  - Cardiopulmonary alterations in mRNA expression for interleukin-1beta, the 
      interleukin-6 superfamily and CXC-chemokines during development of postischaemic 
      heart failure in the rat.
PG  - 263-8
AB  - Cytokines and chemokines are believed to play a pathogenic role in heart failure 
      (HF). Although some cytokines and chemokines have been examined in HF, 
      information about others is still lacking. We aimed to examine the expression of 
      cytokines belonging to the interleukin (IL)-6 superfamily [IL-6 and ciliary 
      neurotrophic factor (CNTF)], as well as IL-1beta and the CXC-chemokines monocyte 
      chemoattractant protein-1 (MCP-1) and IL-8. We examined their expression in the 
      heart, lung and spleen during development of postischaemic HF 1 and 6 weeks 
      following left coronary artery ligation. Rats, which after myocardial infarction 
      had a left ventricular end-diastolic pressure above 15 mmHg, were considered to 
      be in HF. Sham-operated rats served as controls. A substantial upregulation of 
      cardiac IL-1beta was measured in HF at 1 week, whereas a downregulation was 
      measured in the lungs. At 6 weeks no altered regulation was seen. CNTF was only 
      upregulated in the viable left ventricle at 6 weeks and IL-6 was upregulated in 
      the infarcted region at 1 week. Cardiac MCP-1 was upregulated in the viable and 
      the infarcted region of the failing left ventricle at 1 week, with the highest 
      expression in the latter. In the lung, another pattern of regulation was seen 
      with a significant increase in pulmonary MCP-1 at 6 weeks. IL-8 was only detected 
      in the infarcted region at 1 week. In the spleen, no regulation of cytokines was 
      found. In conclusion, we report an organ-specific regulation of cytokines and 
      chemokines in postischaemic HF. Our novel findings of increased cardiac CNTF and 
      cardiopulmonary MCP-1 mRNA indicate a role for these factors in the pathogenesis 
      of HF.
FAU - Tonnessen, Theis
AU  - Tonnessen T
AD  - Department of Cardiothoracic Surgery and Institute for Experimental Medical 
      Research, University of Oslo, Ulleval University Hospital, Oslo, Norway. 
      theis.tonnesen@ioks.uio.no
FAU - Florholmen, Geir
AU  - Florholmen G
FAU - Henriksen, Unni Lie
AU  - Henriksen UL
FAU - Christensen, Geir
AU  - Christensen G
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Clin Physiol Funct Imaging
JT  - Clinical physiology and functional imaging
JID - 101137604
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokines, CXC)
RN  - 0 (Ciliary Neurotrophic Factor)
RN  - 0 (Interleukin-1)
RN  - 0 (Interleukin-6)
RN  - 0 (RNA, Messenger)
SB  - IM
MH  - Animals
MH  - Blotting, Northern
MH  - Body Weight
MH  - Cardiac Output, Low/etiology/*metabolism/pathology/physiopathology
MH  - Chemokine CCL2/genetics
MH  - Chemokines, CXC/genetics/*metabolism
MH  - Ciliary Neurotrophic Factor/genetics
MH  - Hemodynamics
MH  - Interleukin-1/genetics/*metabolism
MH  - Interleukin-6/genetics/*metabolism
MH  - Lung/*metabolism/pathology
MH  - Male
MH  - Myocardial Ischemia/*complications
MH  - Myocardium/*metabolism
MH  - Organ Size
MH  - RNA, Messenger/metabolism
MH  - Rats
MH  - Rats, Wistar
MH  - Up-Regulation
EDAT- 2003/09/03 05:00
MHDA- 2004/04/22 05:00
CRDT- 2003/09/03 05:00
PHST- 2003/09/03 05:00 [pubmed]
PHST- 2004/04/22 05:00 [medline]
PHST- 2003/09/03 05:00 [entrez]
AID - 503 [pii]
AID - 10.1046/j.1475-097x.2003.00503.x [doi]
PST - ppublish
SO  - Clin Physiol Funct Imaging. 2003 Sep;23(5):263-8. doi: 
      10.1046/j.1475-097x.2003.00503.x.