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Effects of G-CSF on cardiac remodeling and arterial hyperplasia in rats.
Eur J Pharmacol. 2006 Nov 07; 549(1-3):98-106.EJ

Abstract

Although granulocyte colony-stimulating factor (G-CSF) has been shown to prevent cardiac remodeling after acute myocardial infarction, the mechanism and safety of G-CSF treatment acute myocardial infarction remain controversial. The purpose of the present study was to investigate in a rat model the mechanisms underlying the beneficial effect of G-CSF in acute myocardial infarction and to determine whether G-CSF treatment aggravates vascular remodeling of injured artery after acute myocardial infarction. Sprague-Dawley rats received transplanted bone marrow cells from green fluorescent protein (GFP) transgenic rats. Acute myocardial infarction was induced by ligation of the left coronary artery. After 24 h, the right carotid artery was injured with a balloon catheter. G-CSF (100 microg/kg/day) or saline was injected subcutaneously for 5 consecutive days after induction of acute myocardial infarction. G-CSF treatment significantly improved left ventricle function and reduced infarct size in rats with acute myocardial infarction. Expression of mRNA for the angiogenic cytokines was significantly higher in the infarction border area in the G-CSF group than in the control group. The surviving cardiomyocytes in infarction area were more in the G-CSF group. GFP-positive cells were gathered in the infarction border area in both groups; G-CSF did not increase cardiac homing of GFP-positive bone marrow cells in contrast to control group. Most GFP-positive cells were CD68-positive (macrophages). It was difficult to find bone marrow-derived cardiomyocytes in the infarcted area. G-CSF treatment inhibited neointima formation and increased reendothelialization of the injured artery. GFP-positive cells were identified most in the adventitia of the injured artery. A few cells in the neointima and reendothelialization were GFP positive. In conclusion, administration of G-CSF appears to be effective for treatment of left ventricular remodeling after acute myocardial infarction and does not aggravate vascular remodeling. The effect of G-CSF on cardiac and vascular remodeling may occur mainly through a direct action on the heart and arteries.

Authors+Show Affiliations

Department of Internal Medicine, Nihon University School of Medicine, Tokyo 173-8610, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

16979158

Citation

Li, Yuxin, et al. "Effects of G-CSF On Cardiac Remodeling and Arterial Hyperplasia in Rats." European Journal of Pharmacology, vol. 549, no. 1-3, 2006, pp. 98-106.
Li Y, Fukuda N, Yokoyama S, et al. Effects of G-CSF on cardiac remodeling and arterial hyperplasia in rats. Eur J Pharmacol. 2006;549(1-3):98-106.
Li, Y., Fukuda, N., Yokoyama, S., Kusumi, Y., Hagikura, K., Kawano, T., Takayama, T., Matsumoto, T., Satomi, A., Honye, J., Mugishima, H., Mitsumata, M., & Saito, S. (2006). Effects of G-CSF on cardiac remodeling and arterial hyperplasia in rats. European Journal of Pharmacology, 549(1-3), 98-106.
Li Y, et al. Effects of G-CSF On Cardiac Remodeling and Arterial Hyperplasia in Rats. Eur J Pharmacol. 2006 Nov 7;549(1-3):98-106. PubMed PMID: 16979158.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Effects of G-CSF on cardiac remodeling and arterial hyperplasia in rats. AU - Li,Yuxin, AU - Fukuda,Noboru, AU - Yokoyama,Shin-Ichiro, AU - Kusumi,Yoshiaki, AU - Hagikura,Kazuhiro, AU - Kawano,Taro, AU - Takayama,Tadateru, AU - Matsumoto,Taro, AU - Satomi,Aya, AU - Honye,Junko, AU - Mugishima,Hideo, AU - Mitsumata,Masako, AU - Saito,Satoshi, Y1 - 2006/08/15/ PY - 2006/03/16/received PY - 2006/07/26/revised PY - 2006/08/02/accepted PY - 2006/9/19/pubmed PY - 2007/1/31/medline PY - 2006/9/19/entrez SP - 98 EP - 106 JF - European journal of pharmacology JO - Eur J Pharmacol VL - 549 IS - 1-3 N2 - Although granulocyte colony-stimulating factor (G-CSF) has been shown to prevent cardiac remodeling after acute myocardial infarction, the mechanism and safety of G-CSF treatment acute myocardial infarction remain controversial. The purpose of the present study was to investigate in a rat model the mechanisms underlying the beneficial effect of G-CSF in acute myocardial infarction and to determine whether G-CSF treatment aggravates vascular remodeling of injured artery after acute myocardial infarction. Sprague-Dawley rats received transplanted bone marrow cells from green fluorescent protein (GFP) transgenic rats. Acute myocardial infarction was induced by ligation of the left coronary artery. After 24 h, the right carotid artery was injured with a balloon catheter. G-CSF (100 microg/kg/day) or saline was injected subcutaneously for 5 consecutive days after induction of acute myocardial infarction. G-CSF treatment significantly improved left ventricle function and reduced infarct size in rats with acute myocardial infarction. Expression of mRNA for the angiogenic cytokines was significantly higher in the infarction border area in the G-CSF group than in the control group. The surviving cardiomyocytes in infarction area were more in the G-CSF group. GFP-positive cells were gathered in the infarction border area in both groups; G-CSF did not increase cardiac homing of GFP-positive bone marrow cells in contrast to control group. Most GFP-positive cells were CD68-positive (macrophages). It was difficult to find bone marrow-derived cardiomyocytes in the infarcted area. G-CSF treatment inhibited neointima formation and increased reendothelialization of the injured artery. GFP-positive cells were identified most in the adventitia of the injured artery. A few cells in the neointima and reendothelialization were GFP positive. In conclusion, administration of G-CSF appears to be effective for treatment of left ventricular remodeling after acute myocardial infarction and does not aggravate vascular remodeling. The effect of G-CSF on cardiac and vascular remodeling may occur mainly through a direct action on the heart and arteries. SN - 0014-2999 UR - https://www.unboundmedicine.com/medline/citation/16979158/Effects_of_G_CSF_on_cardiac_remodeling_and_arterial_hyperplasia_in_rats_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014-2999(06)00829-6 DB - PRIME DP - Unbound Medicine ER -