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Published on: December 2, 2016
Effects of G-CSF on cardiac remodeling and arterial hyperplasia in rats
Yuxin Li1, Noboru Fukuda, Shin-Ichiro Yokoyama
1Department of Internal Medicine, Nihon University School of Medicine, Tokyo 173-8610, Japan.
Insights
Granulocyte colony-stimulating factor (G-CSF) treatment improves heart function and reduces cardiac damage after myocardial infarction in rats. G-CSF also prevents adverse vascular remodeling in injured arteries, suggesting direct beneficial effects.
Area of Science:
- Cardiovascular Research
- Regenerative Medicine
- Cell Biology
Background:
- Granulocyte colony-stimulating factor (G-CSF) is explored for its potential to prevent cardiac remodeling post-myocardial infarction.
- However, the precise mechanisms and safety, particularly regarding vascular remodeling, remain controversial.
Purpose of the Study:
- To investigate the mechanisms of G-CSF's beneficial effects in acute myocardial infarction (AMI) using a rat model.
- To determine if G-CSF treatment exacerbates vascular remodeling in injured arteries following AMI.
Main Methods:
- Sprague-Dawley rats received bone marrow cells from green fluorescent protein (GFP) transgenic rats.
- AMI was induced via left coronary artery ligation, followed by balloon angioplasty of the carotid artery.
- G-CSF or saline was administered subcutaneously for 5 days post-AMI.
Main Results:
- G-CSF treatment significantly improved left ventricle function and reduced infarct size.
- Increased expression of angiogenic cytokines and enhanced survival of cardiomyocytes were observed in the G-CSF group.
- G-CSF inhibited neointima formation and promoted reendothelialization in injured arteries, without increasing cardiac cell homing.
Conclusions:
- G-CSF administration is effective in treating left ventricular remodeling after AMI and does not worsen vascular remodeling.
- The therapeutic effects of G-CSF on cardiac and vascular remodeling likely stem from direct actions on heart and artery tissues.
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.
