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Protective role of 5-azacytidine on myocardial infarction is associated with modulation of macrophage phenotype and inhibition of fibrosis.

Kim YS, Kang WS, Kwon JS, Hong MH, Jeong HY, Jeong HC, Jeong MH, Ahn Y - J. Cell. Mol. Med. (2014)

Bottom Line: Nitric oxide was produced by PGN, which was reduced by 77.87% after 5AZ treatment.Ejection fraction (59.00 ± 8.03% versus 42.52 ± 2.58%), contractility (LV dP/dt-max, 8299.76 ± 411.56 mmHg versus 6610.36 ± 282.37 mmHg) and relaxation indices (LV dP/dt-min, -4661.37 ± 210.73 mmHg versus -4219.50 ± 162.98 mmHg) were improved after 5AZ administration.Cardiac fibrosis in the MI+5AZ was 8.14 ± 1.00%, compared with 14.93 ± 2.98% in the MI group (P < 0.05).

View Article: PubMed Central - PubMed

Affiliation: Heart Research Center, Chonnam National University Hospital, Gwangju, South Korea.

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Related in: MedlinePlus

Effect of 5AZ administration on fibrosis and macrophage phenotypes in infarcted myocardium. (A) Myocardial infarction (MI) was induced and infarct size was measured after 1 day. There was no difference between the MI+saline group and the MI+5AZ group. (B) Cardiac fibrosis induced by myocardial infarction was reduced by 5AZ administration. Two weeks after myocardial infarction, fibrosis was evaluated by Masson's trichrome staining. Fibrotic changes were detected as blue colour and were quantified for expression as a graph. (C) Infiltrated CD68(+) macrophages in infarcted myocardium were counted and the cell numbers were expressed in a graph. (D) iNOS-expressing CD68(+) macrophages were observed in infarcted myocardium, but were significantly reduced by 5AZ administration (upper panels). Arginase-1 (Arg1)-expressing CD68(+) macrophages were predominant in 5AZ- administered infarcted myocardium (lower panels). The iNOS or Arg1-expressing CD68(+) macrophages were calculated and expressed as bar graphs. *P < 0.05 versus MI group; scale bar: 500 μm.
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fig04: Effect of 5AZ administration on fibrosis and macrophage phenotypes in infarcted myocardium. (A) Myocardial infarction (MI) was induced and infarct size was measured after 1 day. There was no difference between the MI+saline group and the MI+5AZ group. (B) Cardiac fibrosis induced by myocardial infarction was reduced by 5AZ administration. Two weeks after myocardial infarction, fibrosis was evaluated by Masson's trichrome staining. Fibrotic changes were detected as blue colour and were quantified for expression as a graph. (C) Infiltrated CD68(+) macrophages in infarcted myocardium were counted and the cell numbers were expressed in a graph. (D) iNOS-expressing CD68(+) macrophages were observed in infarcted myocardium, but were significantly reduced by 5AZ administration (upper panels). Arginase-1 (Arg1)-expressing CD68(+) macrophages were predominant in 5AZ- administered infarcted myocardium (lower panels). The iNOS or Arg1-expressing CD68(+) macrophages were calculated and expressed as bar graphs. *P < 0.05 versus MI group; scale bar: 500 μm.

Mentions: To investigate the role of 5AZ in MI, MI was induced by permanent ligation of the left anterior descending coronary artery in rats. To confirm whether the surgery was induced similar MI in all animals, infarct size was assessed at 24 hrs. Infarct size was similar in the two groups (Fig.4A). Then, 5AZ or saline was administered, and heart tissue was harvested 2 weeks after MI. Cardiac fibrosis was reduced to 8.14 ± 1.00% by 5AZ administration from 14.93 ± 2.98% (Fig.4B).


Protective role of 5-azacytidine on myocardial infarction is associated with modulation of macrophage phenotype and inhibition of fibrosis.

Kim YS, Kang WS, Kwon JS, Hong MH, Jeong HY, Jeong HC, Jeong MH, Ahn Y - J. Cell. Mol. Med. (2014)

Effect of 5AZ administration on fibrosis and macrophage phenotypes in infarcted myocardium. (A) Myocardial infarction (MI) was induced and infarct size was measured after 1 day. There was no difference between the MI+saline group and the MI+5AZ group. (B) Cardiac fibrosis induced by myocardial infarction was reduced by 5AZ administration. Two weeks after myocardial infarction, fibrosis was evaluated by Masson's trichrome staining. Fibrotic changes were detected as blue colour and were quantified for expression as a graph. (C) Infiltrated CD68(+) macrophages in infarcted myocardium were counted and the cell numbers were expressed in a graph. (D) iNOS-expressing CD68(+) macrophages were observed in infarcted myocardium, but were significantly reduced by 5AZ administration (upper panels). Arginase-1 (Arg1)-expressing CD68(+) macrophages were predominant in 5AZ- administered infarcted myocardium (lower panels). The iNOS or Arg1-expressing CD68(+) macrophages were calculated and expressed as bar graphs. *P < 0.05 versus MI group; scale bar: 500 μm.
© Copyright Policy - open-access
Related In: Results  -  Collection

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fig04: Effect of 5AZ administration on fibrosis and macrophage phenotypes in infarcted myocardium. (A) Myocardial infarction (MI) was induced and infarct size was measured after 1 day. There was no difference between the MI+saline group and the MI+5AZ group. (B) Cardiac fibrosis induced by myocardial infarction was reduced by 5AZ administration. Two weeks after myocardial infarction, fibrosis was evaluated by Masson's trichrome staining. Fibrotic changes were detected as blue colour and were quantified for expression as a graph. (C) Infiltrated CD68(+) macrophages in infarcted myocardium were counted and the cell numbers were expressed in a graph. (D) iNOS-expressing CD68(+) macrophages were observed in infarcted myocardium, but were significantly reduced by 5AZ administration (upper panels). Arginase-1 (Arg1)-expressing CD68(+) macrophages were predominant in 5AZ- administered infarcted myocardium (lower panels). The iNOS or Arg1-expressing CD68(+) macrophages were calculated and expressed as bar graphs. *P < 0.05 versus MI group; scale bar: 500 μm.
Mentions: To investigate the role of 5AZ in MI, MI was induced by permanent ligation of the left anterior descending coronary artery in rats. To confirm whether the surgery was induced similar MI in all animals, infarct size was assessed at 24 hrs. Infarct size was similar in the two groups (Fig.4A). Then, 5AZ or saline was administered, and heart tissue was harvested 2 weeks after MI. Cardiac fibrosis was reduced to 8.14 ± 1.00% by 5AZ administration from 14.93 ± 2.98% (Fig.4B).

Bottom Line: Nitric oxide was produced by PGN, which was reduced by 77.87% after 5AZ treatment.Ejection fraction (59.00 ± 8.03% versus 42.52 ± 2.58%), contractility (LV dP/dt-max, 8299.76 ± 411.56 mmHg versus 6610.36 ± 282.37 mmHg) and relaxation indices (LV dP/dt-min, -4661.37 ± 210.73 mmHg versus -4219.50 ± 162.98 mmHg) were improved after 5AZ administration.Cardiac fibrosis in the MI+5AZ was 8.14 ± 1.00%, compared with 14.93 ± 2.98% in the MI group (P < 0.05).

View Article: PubMed Central - PubMed

Affiliation: Heart Research Center, Chonnam National University Hospital, Gwangju, South Korea.

Show MeSH
Related in: MedlinePlus