Effect of granulocyte-macrophage colony-stimulating factor inducer on left ventricular remodeling after acute myocardial infarction

Yuichiro Maekawa, Toshihisa Anzai, Tsutomu Yoshikawa, Yasuo Sugano, Keitaro Mahara, Takashi Kohno, Toshiyuki Takahashi, Satoshi Ogawa

Research output: Contribution to journalArticle

97 Citations (Scopus)

Abstract

We sought to determine the influence of granulocyte-macrophage colony-stimulating factor (GM-CSF) induction on post-myocardial infarction (MI) remodeling, especially in relation to the inflammatory response and myocardial fibrosis. Granulocyte-macrophage colony-stimulating factor modifies wound healing by promoting monocytopoiesis and infiltration of monocytes and macrophages into injured tissue; however, the effect of GM-CSF induction on the infarct healing process and myocardial fibrosis is unclear. A model of MI was produced in Wistar rats by ligation of the left coronary artery. The MI animals were randomized to receive GM-CSF inducer (romurtide 200 μg/kg/day for 7 consecutive days) (MI/Ro) or saline (MI/C). Echocardiographic and hemodynamic studies on day 14 revealed increased left ventricular (LV) end-diastolic dimension, decreased fractional shortening, elevated LV end-diastolic pressure, and decreased LV maximum rate of isovolumic pressure development in MI/Ro compared with MI/C. Immunoblotting showed that expression of transforming growth factor (TGF)-β1 in the infarcted site on day 3 after MI was decreased in MI/Ro compared with MI/C. In the infarcted site, TGF-β1, collagen type I and type III messenger ribonucleic acid (mRNA) expression on day 3, and collagen content on day 7 were reduced in MI/Ro compared with MI/C, in association with marked infarct expansion. In MI/Ro, monocyte chemoattractant protein-1 mRNA level and the degree of infiltration of monocyte-derived macrophages (ED-1-positive)were greater in the infarcted site on day 7 than those in MI/C. The GM-CSF induction by romurtide facilitated infarct expansion in association with the promotion of monocyte recruitment and inappropriate collagen synthesis in the infarcted region during the early phase of MI.

Original languageEnglish
Pages (from-to)1510-1520
Number of pages11
JournalJournal of the American College of Cardiology
Volume44
Issue number7
DOIs
Publication statusPublished - 2004 Oct 6

Fingerprint

Ventricular Remodeling
Granulocyte-Macrophage Colony-Stimulating Factor
Myocardial Infarction
Transforming Growth Factors
Monocytes
Fibrosis
Collagen
Macrophages
RNA
Chemokine CCL2
Collagen Type I
Immunoblotting
Wound Healing

ASJC Scopus subject areas

  • Nursing(all)

Cite this

Effect of granulocyte-macrophage colony-stimulating factor inducer on left ventricular remodeling after acute myocardial infarction. / Maekawa, Yuichiro; Anzai, Toshihisa; Yoshikawa, Tsutomu; Sugano, Yasuo; Mahara, Keitaro; Kohno, Takashi; Takahashi, Toshiyuki; Ogawa, Satoshi.

In: Journal of the American College of Cardiology, Vol. 44, No. 7, 06.10.2004, p. 1510-1520.

Research output: Contribution to journalArticle

Maekawa, Yuichiro ; Anzai, Toshihisa ; Yoshikawa, Tsutomu ; Sugano, Yasuo ; Mahara, Keitaro ; Kohno, Takashi ; Takahashi, Toshiyuki ; Ogawa, Satoshi. / Effect of granulocyte-macrophage colony-stimulating factor inducer on left ventricular remodeling after acute myocardial infarction. In: Journal of the American College of Cardiology. 2004 ; Vol. 44, No. 7. pp. 1510-1520.
@article{48482bc85e744361aaf9566cab174df1,
title = "Effect of granulocyte-macrophage colony-stimulating factor inducer on left ventricular remodeling after acute myocardial infarction",
abstract = "We sought to determine the influence of granulocyte-macrophage colony-stimulating factor (GM-CSF) induction on post-myocardial infarction (MI) remodeling, especially in relation to the inflammatory response and myocardial fibrosis. Granulocyte-macrophage colony-stimulating factor modifies wound healing by promoting monocytopoiesis and infiltration of monocytes and macrophages into injured tissue; however, the effect of GM-CSF induction on the infarct healing process and myocardial fibrosis is unclear. A model of MI was produced in Wistar rats by ligation of the left coronary artery. The MI animals were randomized to receive GM-CSF inducer (romurtide 200 μg/kg/day for 7 consecutive days) (MI/Ro) or saline (MI/C). Echocardiographic and hemodynamic studies on day 14 revealed increased left ventricular (LV) end-diastolic dimension, decreased fractional shortening, elevated LV end-diastolic pressure, and decreased LV maximum rate of isovolumic pressure development in MI/Ro compared with MI/C. Immunoblotting showed that expression of transforming growth factor (TGF)-β1 in the infarcted site on day 3 after MI was decreased in MI/Ro compared with MI/C. In the infarcted site, TGF-β1, collagen type I and type III messenger ribonucleic acid (mRNA) expression on day 3, and collagen content on day 7 were reduced in MI/Ro compared with MI/C, in association with marked infarct expansion. In MI/Ro, monocyte chemoattractant protein-1 mRNA level and the degree of infiltration of monocyte-derived macrophages (ED-1-positive)were greater in the infarcted site on day 7 than those in MI/C. The GM-CSF induction by romurtide facilitated infarct expansion in association with the promotion of monocyte recruitment and inappropriate collagen synthesis in the infarcted region during the early phase of MI.",
author = "Yuichiro Maekawa and Toshihisa Anzai and Tsutomu Yoshikawa and Yasuo Sugano and Keitaro Mahara and Takashi Kohno and Toshiyuki Takahashi and Satoshi Ogawa",
year = "2004",
month = "10",
day = "6",
doi = "10.1016/j.jacc.2004.05.083",
language = "English",
volume = "44",
pages = "1510--1520",
journal = "Journal of the American College of Cardiology",
issn = "0735-1097",
publisher = "Elsevier USA",
number = "7",

}

TY - JOUR

T1 - Effect of granulocyte-macrophage colony-stimulating factor inducer on left ventricular remodeling after acute myocardial infarction

AU - Maekawa, Yuichiro

AU - Anzai, Toshihisa

AU - Yoshikawa, Tsutomu

AU - Sugano, Yasuo

AU - Mahara, Keitaro

AU - Kohno, Takashi

AU - Takahashi, Toshiyuki

AU - Ogawa, Satoshi

PY - 2004/10/6

Y1 - 2004/10/6

N2 - We sought to determine the influence of granulocyte-macrophage colony-stimulating factor (GM-CSF) induction on post-myocardial infarction (MI) remodeling, especially in relation to the inflammatory response and myocardial fibrosis. Granulocyte-macrophage colony-stimulating factor modifies wound healing by promoting monocytopoiesis and infiltration of monocytes and macrophages into injured tissue; however, the effect of GM-CSF induction on the infarct healing process and myocardial fibrosis is unclear. A model of MI was produced in Wistar rats by ligation of the left coronary artery. The MI animals were randomized to receive GM-CSF inducer (romurtide 200 μg/kg/day for 7 consecutive days) (MI/Ro) or saline (MI/C). Echocardiographic and hemodynamic studies on day 14 revealed increased left ventricular (LV) end-diastolic dimension, decreased fractional shortening, elevated LV end-diastolic pressure, and decreased LV maximum rate of isovolumic pressure development in MI/Ro compared with MI/C. Immunoblotting showed that expression of transforming growth factor (TGF)-β1 in the infarcted site on day 3 after MI was decreased in MI/Ro compared with MI/C. In the infarcted site, TGF-β1, collagen type I and type III messenger ribonucleic acid (mRNA) expression on day 3, and collagen content on day 7 were reduced in MI/Ro compared with MI/C, in association with marked infarct expansion. In MI/Ro, monocyte chemoattractant protein-1 mRNA level and the degree of infiltration of monocyte-derived macrophages (ED-1-positive)were greater in the infarcted site on day 7 than those in MI/C. The GM-CSF induction by romurtide facilitated infarct expansion in association with the promotion of monocyte recruitment and inappropriate collagen synthesis in the infarcted region during the early phase of MI.

AB - We sought to determine the influence of granulocyte-macrophage colony-stimulating factor (GM-CSF) induction on post-myocardial infarction (MI) remodeling, especially in relation to the inflammatory response and myocardial fibrosis. Granulocyte-macrophage colony-stimulating factor modifies wound healing by promoting monocytopoiesis and infiltration of monocytes and macrophages into injured tissue; however, the effect of GM-CSF induction on the infarct healing process and myocardial fibrosis is unclear. A model of MI was produced in Wistar rats by ligation of the left coronary artery. The MI animals were randomized to receive GM-CSF inducer (romurtide 200 μg/kg/day for 7 consecutive days) (MI/Ro) or saline (MI/C). Echocardiographic and hemodynamic studies on day 14 revealed increased left ventricular (LV) end-diastolic dimension, decreased fractional shortening, elevated LV end-diastolic pressure, and decreased LV maximum rate of isovolumic pressure development in MI/Ro compared with MI/C. Immunoblotting showed that expression of transforming growth factor (TGF)-β1 in the infarcted site on day 3 after MI was decreased in MI/Ro compared with MI/C. In the infarcted site, TGF-β1, collagen type I and type III messenger ribonucleic acid (mRNA) expression on day 3, and collagen content on day 7 were reduced in MI/Ro compared with MI/C, in association with marked infarct expansion. In MI/Ro, monocyte chemoattractant protein-1 mRNA level and the degree of infiltration of monocyte-derived macrophages (ED-1-positive)were greater in the infarcted site on day 7 than those in MI/C. The GM-CSF induction by romurtide facilitated infarct expansion in association with the promotion of monocyte recruitment and inappropriate collagen synthesis in the infarcted region during the early phase of MI.

UR - http://www.scopus.com/inward/record.url?scp=4644296825&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=4644296825&partnerID=8YFLogxK

U2 - 10.1016/j.jacc.2004.05.083

DO - 10.1016/j.jacc.2004.05.083

M3 - Article

C2 - 15464336

AN - SCOPUS:4644296825

VL - 44

SP - 1510

EP - 1520

JO - Journal of the American College of Cardiology

JF - Journal of the American College of Cardiology

SN - 0735-1097

IS - 7

ER -