TY - JOUR
T1 - Versican is induced in infiltrating monocytes in myocardial infarction
AU - Toeda, Kenichi
AU - Nakamura, Keigo
AU - Hirohata, Satoshi
AU - Hatipoglu, Omer F.
AU - Demircan, Kadir
AU - Yamawaki, Hitoshi
AU - Ogawa, Hiroko
AU - Kusachi, Shozo
AU - Shiratori, Yasushi
AU - Ninomiya, Yoshifumi
N1 - Funding Information:
The authors would like to thank Dr. Toshitaka Oohashi, Dr. Tomoko Yonezawa, Ms. Yoko Bekku, Dr. Aiji Ohtsuka and other members of our department for stimulating discussions and help. The authors are also grateful to Mr. Tomoaki Okamoto, Ms. Tomoko Maeda, and Ms. Kahori Tanaka for technical help. This work was supported in part by funding from grants-in-aid for Scientific Research from the Japan Society for the Promotion of Science (grants 15390459 to S.H. and 16591755 to S.K.).
PY - 2005/12
Y1 - 2005/12
N2 - Versican, a large chondroitin sulfate proteoglycan, plays a role in conditions such as wound healing and tissue remodelling. To test the hypothesis that versican expression is transiently upregulated and plays a role in the infarcted heart, we examined its expression in a rat model of myocardial infarction. Northern blot analysis demonstrated increased expression of versican mRNA. Quantitative real-time RT-PCR analysis revealed that versican mRNA began to increase as early as 6 h and reached its maximal level 2 days after coronary artery ligation. Versican mRNA then gradually decreased, while the mRNA of decorin, another small proteoglycan, increased thereafter. Versican mRNA was localized in monocytes, as indicated by CD68-positive staining, around the infarct tissue. The induction of versican mRNA was accelerated by ischemia/reperfusion (I/R), which was characterized by massive cell infiltration and enhanced inflammatory response. To examine the alteration of versican expression in monocytes/macrophages, we isolated human peripheral blood mononuclear cells and stimulated them with granulocyte/macrophage colony-stimulating factor (GM-CSF). Stimulation of mononuclear cells with GM-CSF increased the expression of versican mRNA as well as cytokine induction. The production of versican by monocytes in the infarct area represents a novel finding of the expression of an extracellular matrix gene by monocytes in the infarcted heart. We suggest that upregulation of versican in the infarcted myocardium may have a role in the inflammatory reaction, which mediates subsequent chemotaxis in the infarcted heart.
AB - Versican, a large chondroitin sulfate proteoglycan, plays a role in conditions such as wound healing and tissue remodelling. To test the hypothesis that versican expression is transiently upregulated and plays a role in the infarcted heart, we examined its expression in a rat model of myocardial infarction. Northern blot analysis demonstrated increased expression of versican mRNA. Quantitative real-time RT-PCR analysis revealed that versican mRNA began to increase as early as 6 h and reached its maximal level 2 days after coronary artery ligation. Versican mRNA then gradually decreased, while the mRNA of decorin, another small proteoglycan, increased thereafter. Versican mRNA was localized in monocytes, as indicated by CD68-positive staining, around the infarct tissue. The induction of versican mRNA was accelerated by ischemia/reperfusion (I/R), which was characterized by massive cell infiltration and enhanced inflammatory response. To examine the alteration of versican expression in monocytes/macrophages, we isolated human peripheral blood mononuclear cells and stimulated them with granulocyte/macrophage colony-stimulating factor (GM-CSF). Stimulation of mononuclear cells with GM-CSF increased the expression of versican mRNA as well as cytokine induction. The production of versican by monocytes in the infarct area represents a novel finding of the expression of an extracellular matrix gene by monocytes in the infarcted heart. We suggest that upregulation of versican in the infarcted myocardium may have a role in the inflammatory reaction, which mediates subsequent chemotaxis in the infarcted heart.
KW - Coronary artery disease
KW - Cytokine
KW - Extracellular matrix
KW - GM-CSF
KW - Monocyte
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U2 - 10.1007/s11010-005-8051-4
DO - 10.1007/s11010-005-8051-4
M3 - Article
C2 - 16311904
AN - SCOPUS:27144493818
SN - 0300-8177
VL - 280
SP - 47
EP - 56
JO - Molecular and Cellular Biochemistry
JF - Molecular and Cellular Biochemistry
IS - 1-2
ER -