지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
커뮤니티
연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2011.1
- 수록면
- 48 - 56 (9page)
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초록· 키워드
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Background: Hypertensive myocardial fibrosis promotes abnormalities of cardiac function that may adversely affect the clinical outcome of hypertensive patients. Imatinib mesylate blocks receptor tyrosine kinase and is clinically used to treat leukemia.
Platelet-derived growth factor (PDGF) is a downstream target of receptor tyrosine kinases. Cardiac fibroblasts can be activated by PDGF. Thus we evaluated whether imatinib attenuate myocardial fibrosis and prevents diastolic dysfunction in spontaneously hypertensive rats (SHR). Methods: 8 weeks old male SHRs were subjected to treatment with 8 weeks of low dose imatinib (SHR-10; 10 mg/kg), high dose imatinib (SHR-30; 30 mg/kg) or saline (SHR-C; n = 6 in each group). At the age of 16 weeks,all rats underwent hemodynamic studies and Doppler echocardiography, and were sacrificed. Their hearts were extracted for histopathological, immunoblotting and quantitative reverse transcriptase-polymerase chain reaction analyses. Results: While imatinib did not affect blood pressure (BP), it markedly reduced perivascular and interstitial fibrosis in the hearts of SHR.
Echocardigram showed that high-dose imatinib significantly reduced left ventricular (LV) wall thickness (septal/posterior wall;SHR-C vs. SHR-30: 18 ± 2/19 ± 2 mm vs. 15 ± 1/14 ± 1 mm; p < 0.05) and improved the parameters of LV diastolic function such as E/A ratio (SHR-C vs. SHR-30: 1.60 ± 0.10 vs. 1.86 ± 0.20; p < 0.05). Imatinib also significantly reduced mRNA expression of collagen III and PDGF β-receptor tyrosine phosphorylation in the hearts of SHR. Conclusions: These results suggest that imatinib, especially high dose, could attenuate myocardial fibrosis and prevent LV diastolic dysfunction in hypertensive rat model by decreased activity of PDGF. Imatinib may provide a potential therapeutic approach for hypertensive heart disease.
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참고문헌 (22)
참고문헌 신청
Abdollahi A / 2005 / Inhibition of platelet-derived growth factor signaling attenuates pulmonary fibrosis / Journal of Experimental Medicine 201 : 925 ~ 935
Aono Y / 2005 / Imatinib as a novel antifibrotic agent in bleomycin-induced pulmonary fibrosis in mice / American Journal of Respiratory and Critical Care Medicine 171 : 127
Bing OH / 1995 / The spontaneously hypertensive rat as a model of the transition from compensated left ventricular hypertrophy to failure / Journal of Molecular and Cellular
Bryant D / 1998 / Cardiac failure in transgenic mice with myocardial expression of tumor necrosis factor-alpha / Circulation 98 : 1375 ~ 1381
Cingolani OH / 2004 / Carretero OA. Reduction of cardiac fibrosis decreases systolic performance without affecting diastolic function in hypertensive rats / Hypertension 43
Aono Y / 2005 / Imatinib as a novel antifibrotic agent in bleomycin-induced pulmonary fibrosis in mice / American Journal of Respiratory and Critical Care Medicine 171 : 127
Bing OH / 1995 / The spontaneously hypertensive rat as a model of the transition from compensated left ventricular hypertrophy to failure / Journal of Molecular and Cellular
Bryant D / 1998 / Cardiac failure in transgenic mice with myocardial expression of tumor necrosis factor-alpha / Circulation 98 : 1375 ~ 1381
Cingolani OH / 2004 / Carretero OA. Reduction of cardiac fibrosis decreases systolic performance without affecting diastolic function in hypertensive rats / Hypertension 43
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