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

doi:10.1161/01.CIR.95.3.693

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

Research output: Contribution to journal › Article › peer-review

167 Scopus citations

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 language	English (US)
Pages (from-to)	693-700
Number of pages	8
Journal	Circulation
Volume	95
Issue number	3
DOIs	https://doi.org/10.1161/01.CIR.95.3.693
State	Published - 1997
Externally published	Yes

Keywords

cytokines
myocardial infarction
proteins, monocyte chemoattractant
reperfusion

ASJC Scopus subject areas

Cardiology and Cardiovascular Medicine
Physiology (medical)

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10.1161/01.CIR.95.3.693

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Kumar, A. G., Ballantyne, C. M., Michael, L. H., Kukielka, G. L., Youker, K. A., Lindsey, M. L., Hawkins, H. K., Birdsall, H. H., MacKay, C. R., LaRosa, G. J., Rossen, R. D., Smith, C. W., & 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. https://doi.org/10.1161/01.CIR.95.3.693

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. https://doi.org/10.1161/01.CIR.95.3.693

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

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.",

keywords = "cytokines, myocardial infarction, proteins, monocyte chemoattractant, reperfusion",

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

year = "1997",

doi = "10.1161/01.CIR.95.3.693",

language = "English (US)",

volume = "95",

pages = "693--700",

journal = "Circulation",

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TY - JOUR

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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U2 - 10.1161/01.CIR.95.3.693

DO - 10.1161/01.CIR.95.3.693

M3 - Article

C2 - 9024159

AN - SCOPUS:16844387569

SN - 0009-7322

VL - 95

SP - 693

EP - 700

JO - Circulation

JF - Circulation

IS - 3

ER -

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

Abstract

Keywords

ASJC Scopus subject areas

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