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The antiapoptotic effect of granulocyte colony-stimulating factor reduces infarct size and prevents heart failure
Marcelo Perim Baldo1, Ana P C Davel, Danilo M Damas-Souza
1Department of Physiological Sciences, Federal University of Espírito Santo, Vitória, Brazil. marcelobaldo@ymail.com
Insights
Granulocyte colony-stimulating factor (G-CSF) reduces heart attack injury and preserves cardiac function in rats. Early G-CSF treatment is essential for long-term benefits after myocardial infarction.
Area of Science:
- Cardiology
- Regenerative Medicine
- Molecular Biology
Background:
- Myocardial infarction (MI) causes significant heart damage.
- Granulocyte colony-stimulating factor (G-CSF) is known to reduce myocardial injury.
- The long-term effects of G-CSF on cardiac function post-MI require further investigation.
Purpose of the Study:
- To investigate the early effects of G-CSF on myocardial injury.
- To evaluate the chronic repercussions of G-CSF treatment on cardiac function in a rat model of MI.
- To understand the molecular mechanisms underlying G-CSF's protective effects.
Main Methods:
- Male Wistar rats underwent MI surgery.
- G-CSF or vehicle was administered pre-MI.
- Infarct size, apoptotic nuclei, protein expression (Bcl-2, Bcl-xL, Bax), and left ventricular function were assessed at various time points.
Main Results:
- G-CSF pre-treatment significantly reduced infarct size at 1 and 15 days post-MI.
- G-CSF increased anti-apoptotic proteins (Bcl-2, Bcl-xL) and decreased apoptotic nuclei.
- Cardiac function was preserved, and LV dilation was reduced in G-CSF treated rats 15 days post-MI.
Conclusions:
- Early G-CSF administration provides sustained cardioprotection after myocardial infarction.
- G-CSF's beneficial effects are linked to reduced apoptosis and preserved cardiac function.
- G-CSF is a promising therapeutic agent for managing myocardial infarction.
Background/Aim:
Granulocyte colony-stimulating factor (G-CSF) reduces myocardial injury and improves cardiac function after myocardial infarction (MI). We investigated the early alterations provided by G-CSF and the chronic repercussions in infarcted rats.
Methods:
Male Wistar rats (200-250g) received vehicle (MI) or G-CSF (MI-GCSF) (50 μg/kg, sc) at 7, 3 and 1 days before MI surgery. Afterwards MI was produced and infarct size was measured 1 and 15 days after surgery. Expression of anti- and proapoptotic proteins was evaluated immediately before surgery. 24 hours after surgery, apoptotic nuclei were evaluated. Two weeks after MI, left ventricular (LV) function was evaluated, followed by in situ LV diastolic pressure-volume evaluation.
Results:
Infarct size was decreased by 1 day pre-treatment before occlusion (36±2.8 vs. 44±2.1% in MI; P<0.05) and remained reduced at 15 days after infarction (28±2.2 vs. 36±1.4% in MI; P<0.05). G-CSF pretreatment increased Bcl-2 and Bcl-xL protein expression, but did not alter Bax in LV. Apoptotic nuclei were reduced by treatment (Sham: 0.46±0.42, MI: 15.5±2.43, MI-GCSF: 5.34±3.34%; P<0.05). Fifteen days after MI, cardiac function remained preserved in G-CSF pretreated rats. The LV dilation was reduced in MI-G-CSF group as compared to MI rats, being closely associated with infarct size.
Conclusion:
The early beneficial effects of G-CSF were essentials to preserve cardiac function at a chronic stage of myocardial infarction.
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