Induction of monocyte chemoattractant protein-1 in the small veins of the ischemic and reperfused canine myocardium

Ajith G. Kumar, Christie M. Ballantyne, Lloyd H. Michael, Gilbert L. Kukielka, Keith A. Youker, Merry L. Lindsey, Hal K. Hawkins, Holly H. Birdsall, Charles R. MacKay, Gregory J. LaRosa, Roger D. Rossen, C. Wayne Smith, Mark L. Entman

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Abstract

Background: Healing after myocardial infarction is characterized by the presence of macrophages in the infarcted area. Since augmented monocyte influx has been implicated as a potential mechanism for improved healing after reperfusion, we wished to study the induction of monocyte chemoattractant protein-1 (MCP-1) during reperfusion. Methods and Results: The cDNA for MCP-1 was cloned from a canine jugular vein endothelial cell (CJVEC) library and exhibited 78% identity with the deduced amino acid sequence of human MCP-1. Samples of myocardium were taken from control and ischemic segments after 1 hour of ischemia and various times of reperfusion: total RNA was isolated from myocardial samples and probed with a cDNA probe for canine MCP-1. Induction of MCP-1 mRNA occurred only in previously ischemic segments within the first hour of reperfusion, peaked at 3 hours, and persisted throughout the first 2 days of reperfusion. In the absence of reperfusion, no significant MCP-1 induction was seen. Both ischemic (but not preischemic) cardiac lymph and human recombinant TNF-α induced MCP-1 in CJVECs. MCP-1 was identified by immunostaining on infiltrating cells and venular (but not arterial) endothelium by 3 hours. In contrast, in situ hybridization showed MCP-1 mRNA to be confined to the endothelium of small veins (venules) 10 to 70 μm in diameter. Conclusions: MCP-1 mRNA is induced in the endothelium of a specific class of small veins immediately after reperfusion. MCP-1 induction is confined to the previously ischemic area that has been reperfused. We suggest a significant role for MCP-1 in monocyte trafficking in the reperfused myocardium.

Original languageEnglish (US)
Pages (from-to)693-700
Number of pages8
JournalCirculation
Volume95
Issue number3
StatePublished - 1997

Fingerprint

Chemokine CCL2
Canidae
Veins
Myocardium
Reperfusion
Endothelium
Messenger RNA
Monocytes
Complementary DNA
Venules
Jugular Veins
Lymph
In Situ Hybridization
Amino Acid Sequence
Ischemia
Endothelial Cells
Macrophages
Myocardial Infarction
RNA

Keywords

  • cytokines
  • myocardial infarction
  • proteins, monocyte chemoattractant
  • reperfusion

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

Kumar, A. G., Ballantyne, C. M., Michael, L. H., Kukielka, G. L., Youker, K. A., Lindsey, M. L., ... Entman, M. L. (1997). Induction of monocyte chemoattractant protein-1 in the small veins of the ischemic and reperfused canine myocardium. Circulation, 95(3), 693-700.

Induction of monocyte chemoattractant protein-1 in the small veins of the ischemic and reperfused canine myocardium. / Kumar, Ajith G.; Ballantyne, Christie M.; Michael, Lloyd H.; Kukielka, Gilbert L.; Youker, Keith A.; Lindsey, Merry L.; Hawkins, Hal K.; Birdsall, Holly H.; MacKay, Charles R.; LaRosa, Gregory J.; Rossen, Roger D.; Smith, C. Wayne; Entman, Mark L.

In: Circulation, Vol. 95, No. 3, 1997, p. 693-700.

Research output: Contribution to journalArticle

Kumar, AG, Ballantyne, CM, Michael, LH, Kukielka, GL, Youker, KA, Lindsey, ML, Hawkins, HK, Birdsall, HH, MacKay, CR, LaRosa, GJ, Rossen, RD, Smith, CW & Entman, ML 1997, 'Induction of monocyte chemoattractant protein-1 in the small veins of the ischemic and reperfused canine myocardium', Circulation, vol. 95, no. 3, pp. 693-700.
Kumar AG, Ballantyne CM, Michael LH, Kukielka GL, Youker KA, Lindsey ML et al. Induction of monocyte chemoattractant protein-1 in the small veins of the ischemic and reperfused canine myocardium. Circulation. 1997;95(3):693-700.
Kumar, Ajith G. ; Ballantyne, Christie M. ; Michael, Lloyd H. ; Kukielka, Gilbert L. ; Youker, Keith A. ; Lindsey, Merry L. ; Hawkins, Hal K. ; Birdsall, Holly H. ; MacKay, Charles R. ; LaRosa, Gregory J. ; Rossen, Roger D. ; Smith, C. Wayne ; Entman, Mark L. / Induction of monocyte chemoattractant protein-1 in the small veins of the ischemic and reperfused canine myocardium. In: Circulation. 1997 ; Vol. 95, No. 3. pp. 693-700.
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abstract = "Background: Healing after myocardial infarction is characterized by the presence of macrophages in the infarcted area. Since augmented monocyte influx has been implicated as a potential mechanism for improved healing after reperfusion, we wished to study the induction of monocyte chemoattractant protein-1 (MCP-1) during reperfusion. Methods and Results: The cDNA for MCP-1 was cloned from a canine jugular vein endothelial cell (CJVEC) library and exhibited 78{\%} identity with the deduced amino acid sequence of human MCP-1. Samples of myocardium were taken from control and ischemic segments after 1 hour of ischemia and various times of reperfusion: total RNA was isolated from myocardial samples and probed with a cDNA probe for canine MCP-1. Induction of MCP-1 mRNA occurred only in previously ischemic segments within the first hour of reperfusion, peaked at 3 hours, and persisted throughout the first 2 days of reperfusion. In the absence of reperfusion, no significant MCP-1 induction was seen. Both ischemic (but not preischemic) cardiac lymph and human recombinant TNF-α induced MCP-1 in CJVECs. MCP-1 was identified by immunostaining on infiltrating cells and venular (but not arterial) endothelium by 3 hours. In contrast, in situ hybridization showed MCP-1 mRNA to be confined to the endothelium of small veins (venules) 10 to 70 μm in diameter. Conclusions: MCP-1 mRNA is induced in the endothelium of a specific class of small veins immediately after reperfusion. MCP-1 induction is confined to the previously ischemic area that has been reperfused. We suggest a significant role for MCP-1 in monocyte trafficking in the reperfused myocardium.",
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T1 - Induction of monocyte chemoattractant protein-1 in the small veins of the ischemic and reperfused canine myocardium

AU - Kumar, Ajith G.

AU - Ballantyne, Christie M.

AU - Michael, Lloyd H.

AU - Kukielka, Gilbert L.

AU - Youker, Keith A.

AU - Lindsey, Merry L.

AU - Hawkins, Hal K.

AU - Birdsall, Holly H.

AU - MacKay, Charles R.

AU - LaRosa, Gregory J.

AU - Rossen, Roger D.

AU - Smith, C. Wayne

AU - Entman, Mark L.

PY - 1997

Y1 - 1997

N2 - Background: Healing after myocardial infarction is characterized by the presence of macrophages in the infarcted area. Since augmented monocyte influx has been implicated as a potential mechanism for improved healing after reperfusion, we wished to study the induction of monocyte chemoattractant protein-1 (MCP-1) during reperfusion. Methods and Results: The cDNA for MCP-1 was cloned from a canine jugular vein endothelial cell (CJVEC) library and exhibited 78% identity with the deduced amino acid sequence of human MCP-1. Samples of myocardium were taken from control and ischemic segments after 1 hour of ischemia and various times of reperfusion: total RNA was isolated from myocardial samples and probed with a cDNA probe for canine MCP-1. Induction of MCP-1 mRNA occurred only in previously ischemic segments within the first hour of reperfusion, peaked at 3 hours, and persisted throughout the first 2 days of reperfusion. In the absence of reperfusion, no significant MCP-1 induction was seen. Both ischemic (but not preischemic) cardiac lymph and human recombinant TNF-α induced MCP-1 in CJVECs. MCP-1 was identified by immunostaining on infiltrating cells and venular (but not arterial) endothelium by 3 hours. In contrast, in situ hybridization showed MCP-1 mRNA to be confined to the endothelium of small veins (venules) 10 to 70 μm in diameter. Conclusions: MCP-1 mRNA is induced in the endothelium of a specific class of small veins immediately after reperfusion. MCP-1 induction is confined to the previously ischemic area that has been reperfused. We suggest a significant role for MCP-1 in monocyte trafficking in the reperfused myocardium.

AB - Background: Healing after myocardial infarction is characterized by the presence of macrophages in the infarcted area. Since augmented monocyte influx has been implicated as a potential mechanism for improved healing after reperfusion, we wished to study the induction of monocyte chemoattractant protein-1 (MCP-1) during reperfusion. Methods and Results: The cDNA for MCP-1 was cloned from a canine jugular vein endothelial cell (CJVEC) library and exhibited 78% identity with the deduced amino acid sequence of human MCP-1. Samples of myocardium were taken from control and ischemic segments after 1 hour of ischemia and various times of reperfusion: total RNA was isolated from myocardial samples and probed with a cDNA probe for canine MCP-1. Induction of MCP-1 mRNA occurred only in previously ischemic segments within the first hour of reperfusion, peaked at 3 hours, and persisted throughout the first 2 days of reperfusion. In the absence of reperfusion, no significant MCP-1 induction was seen. Both ischemic (but not preischemic) cardiac lymph and human recombinant TNF-α induced MCP-1 in CJVECs. MCP-1 was identified by immunostaining on infiltrating cells and venular (but not arterial) endothelium by 3 hours. In contrast, in situ hybridization showed MCP-1 mRNA to be confined to the endothelium of small veins (venules) 10 to 70 μm in diameter. Conclusions: MCP-1 mRNA is induced in the endothelium of a specific class of small veins immediately after reperfusion. MCP-1 induction is confined to the previously ischemic area that has been reperfused. We suggest a significant role for MCP-1 in monocyte trafficking in the reperfused myocardium.

KW - cytokines

KW - myocardial infarction

KW - proteins, monocyte chemoattractant

KW - reperfusion

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VL - 95

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JF - Circulation

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