자주쓰는 링크
작성일 : 14-09-21 12:31
| 연구단계 | 1단계 : 2년차 | ||
| 논문제목(영문) | Protective role of 5-azacytidine on myocardial infarction is associated with modulation of macrophage phenotype and inhibition of fibrosis. | ||
| 국내외구분 | 국외 | SCI여부 | SCI |
| 연구책임자역활 | 교신저자 | 논문기여율 | 30% |
| 주저자명 | Kim YS | ||
| 교신저자명 | Ahn Y | ||
| 공동저자명 | Kang WS, Kwon JS, Hong MH, Jeong HY, Jeong HC, Jeong MH | ||
| 게제년월일 | 2014-06-01 | ||
| ISSN | 1582-4934 | ||
| Impact Factor | 3.698 | ||
| 학술지명 | J Cell Mol Med | ||
| 서지사항 | 0집 / 18권 / 6호, 페이지(1018 - 1027) | ||
| 병기표기 | 단독 | ||
| Acknowledgement 기재여부 |
예
※ Acknowledgement가 기재된 논문만 연구과제의 성과로 인정. - 국문 표기 : "본 연구는 보건복지부 보건의료연구개발사업의 지원에 의하여 이루어진 것임. (HI13C1527)" - 영문 표기 : "This study was supported by a grant of the Korean Health Technology R&D Project, (HI13C1527) Ministry of Health & Welfare, Republic of Korea. " |
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| 요약초록문 (Abstract) 입력 |
We examined whether a shift in macrophage phenotype could be therapeutic for myocardial infarction (MI). The mouse macrophage cell line RAW264.7 was stimulated with peptidoglycan (PGN), with or without 5-azacytidine (5AZ) treatment. MI was induced by ligation of the left anterior descending coronary artery in rats, and the rats were divided into two groups; a saline-injection group and a 5AZ-injection group (2.5 mg/kg/day, intraperitoneal injection). LV function was evaluated and immunohistochemical analyses were performed 2 weeks after MI. Cardiac fibrosis was induced by angiotensin II (AngII) infusion with or without 5AZ (5 mg/kg/day) in mice. Nitric oxide was produced by PGN, which was reduced by 77.87% after 5AZ treatment. Both induction of inducible nitric oxide synthase (iNOS) and iNOS promoter activity by PGN were inhibited by 5AZ. 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). Arginase-1(+)CD68(+) macrophages with anti-inflammatory phenotype were predominant in the infarct border zone of the MI+5AZ group, in comparison with the MI group. AngII-induced cardiac fibrosis was also attenuated after 5AZ administration. In cardiac fibroblasts, pro-fibrotic mediators and cell proliferation were increased by AngII, and these increases were attenuated after 5AZ treatment. 5AZ exerts its cardiac protective role through modulation of macrophages and cardiac fibroblasts. |
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