PMID- 16179730
OWN - NLM
STAT- MEDLINE
DCOM- 20051121
LR  - 20190608
IS  - 1535-3702 (Print)
IS  - 1535-3699 (Linking)
VI  - 230
IP  - 9
DP  - 2005 Oct
TI  - Thrombospondin-1 is induced in rat myocardial infarction and its induction is 
      accelerated by ischemia/reperfusion.
PG  - 621-30
AB  - Thrombospondin-1 (TSP-1) is a multifunctional, rapid-turnover matricellular 
      protein. Recent studies demonstrated that TSP-1 has a role in regulating 
      inflammatory reactions. Myocardial infarction (MI) is associated with an 
      inflammatory response, ultimately leading to healing and scar formation. In 
      particular, an enhanced inflammatory reaction and a massive accumulation of 
      monocytes/macrophages is seen with reperfusion after MI. To examine the role of 
      TSP-1 in MI, we isolated rat TSP-1 complementary DNA (cDNA) and analyzed the 
      level and distribution of the mRNA expression. In infarcted rat hearts, TSP-1 
      mRNA increased markedly at 6 and 12 hrs after coronary artery ligation (27.97 +/- 
      3.40-fold and 22.77 +/- 1.83-fold, respectively, compared with sham-operated 
      hearts). Western blot analysis revealed that TSP-1 protein was transiently 
      induced in the infarcted heart. Using in situ hybridization analysis, TSP-1 mRNA 
      signals were observed in the infiltrating cells at the border area of infarction. 
      We then examined the effect of ischemia/reperfusion (I/R) on TSP-1 mRNA induction 
      in the rats with infarcted hearts. Quantitative reverse transcriptase polymerase 
      chain reaction (RT-PCR) demonstrated that I/R enhanced the TSP-1 mRNA expression 
      approximately 4-fold, as compared with the level in the permanently ligated 
      heart. Finally, we examined the effect of TSP-1 on proinflammatory cytokine 
      release in mononuclear cells. The releases of interleukin-6 (IL-6) and monocyte 
      chemoattractant protein-1 (MCP-1) from human mononuclear cells were enhanced by 
      TSP-1 in a dose-dependent manner. Thus, the immediate and marked increase of 
      TSP-1 expression suggests that TSP-1 has an inflammatory-associated role in MI.
FAU - Sezaki, Satoshi
AU  - Sezaki S
AD  - Department of Medicine and Medical Science, Okayama University Graduate School of 
      Medicine and Dentistry, Okayama, Japan.
FAU - Hirohata, Satoshi
AU  - Hirohata S
FAU - Iwabu, Akihiro
AU  - Iwabu A
FAU - Nakamura, Keigo
AU  - Nakamura K
FAU - Toeda, Kenichi
AU  - Toeda K
FAU - Miyoshi, Toru
AU  - Miyoshi T
FAU - Yamawaki, Hitoshi
AU  - Yamawaki H
FAU - Demircan, Kadir
AU  - Demircan K
FAU - Kusachi, Shozo
AU  - Kusachi S
FAU - Shiratori, Yasushi
AU  - Shiratori Y
FAU - Ninomiya, Yoshifumi
AU  - Ninomiya Y
LA  - eng
SI  - GENBANK/AF309630
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Switzerland
TA  - Exp Biol Med (Maywood)
JT  - Experimental biology and medicine (Maywood, N.J.)
JID - 100973463
RN  - 0 (DNA Primers)
RN  - 0 (DNA, Complementary)
RN  - 0 (RNA, Messenger)
RN  - 0 (Thrombospondin 1)
SB  - IM
MH  - Amino Acid Sequence
MH  - Animals
MH  - Base Sequence
MH  - Blotting, Western
MH  - Cells, Cultured
MH  - Cloning, Molecular
MH  - DNA Primers
MH  - DNA, Complementary
MH  - Immunohistochemistry
MH  - In Situ Hybridization
MH  - Male
MH  - Molecular Sequence Data
MH  - Myocardial Infarction/*metabolism
MH  - RNA, Messenger/genetics
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Reperfusion Injury/*metabolism
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Thrombospondin 1/*biosynthesis/chemistry/genetics
EDAT- 2005/09/24 09:00
MHDA- 2005/12/13 09:00
CRDT- 2005/09/24 09:00
PHST- 2005/09/24 09:00 [pubmed]
PHST- 2005/12/13 09:00 [medline]
PHST- 2005/09/24 09:00 [entrez]
AID - 230/9/621 [pii]
AID - 10.1177/153537020523000904 [doi]
PST - ppublish
SO  - Exp Biol Med (Maywood). 2005 Oct;230(9):621-30. doi: 10.1177/153537020523000904.