Early-phase changes of parameters related to myocardial fibrosis in acute myocardial infarction
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AIM:To investigate the changes in parameters related to myocardial fibrosis of H2 relaxin (H2RLX) and procollagen type I C-terminal peptide (PICP),transforming growth factor-β1 (TGF-β1) level in the plasma after acute anterior myocardial infarction. METHODS:Forty-one patients with anterior myocardial infarction (MI) and 10 controls with normal coronary vessels were selected. Plasma H2RLX,PICP,and TGF-β1 levels were determined by enzyme linked immunosorbent assay (ELISA) in 10 control subjects and 41 post-MI patients at day 3 and 7 post-MI. RESULTS:(1) H2RLX level at day 3 post-infarct had no difference between the patients and the controls. No marked change in H2RLX at day 3 versus day 7 post-infarct was observed. (2)The level of PICP at day 3 post-infarct was markedly increased followed by a fall at day 7 post-infarct,but was still higher than that in control. (3) TGF-β1 level,which was similar at day 3 and 7 post-infarct,was higher than that in control. (4) At day 7 post-infarct,the level of H2RLX was positively correlated with the fasting blood glucose in MI group. CONCLUSION:In early period of acute MI,profibrotic factors such as TGF-β1 expression and collagen expression increase. However,antifibrotic relaxin has no change.Keywords:
Myocardial fibrosis
Relaxin
Procollagen peptidase
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Ventricular remodeling
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Speckle tracking echocardiography
Systole
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AIM: To explore the molecular mechanisms about fibrosis and transforming growth factor (TGF)-β1 as well as inflammation in rats heart after acute myocardial infarction (AMI) . METHODS: AMI model in rats was produced by left coronary artery ligation. Samples of rat cardiac tissue were collected at the end of 1 week, 4 weeks and 8 weeks. Hemodynamics had been performed before rats were sacrificed. Reverse transcription polymerase chain reaction (RT - PCR) and immunohistoche-mical methods were used to analyze mRNA expression and protein production of TGF-β1 , respectively. Hydroxyproline was determined by chloramines T method. HE staining was resorted to analyze pathological myocardium after AMI. RESULTS: There were remarkable differences in hemodynamics between AMI groups and sham group (P0.01) . Compared with sham group, TGF - β1 mRNA expression and protein production and hydroxyproline quantification were enhanced greatly. Among them, the levels of TGF -β1 and hydroxyproline at 1 week were higher than those at 4 weeks or 8 weeks. A positive correlation between TGF-β1 protein and hydroxyproline was presented (r =0.15-0.99, P0.05). In microscope, leucocytes infiltrated significantly in the infarcted and border myocardium at 1 week after AMI, and were rarely seen at 4 weeks and 8 weeks. TGF-β1 protein were detected in cytoplasm of cardiac myocyte and leucocytes at 1 week, and at 4 and 8 weeks in myofibroblast and interstitial. CONCLUSIONS: TGF-β1 is upregulated and found in cytoplasm of cardiac myocyte and leucocytes as well as myofibroblast in heart after AMI, which is associated with dynamic changes of hydroxyproline content and inflammation. TGF -β1 is showed to play an important role in myocardial inflammatory repair and ventricular remodeling after AMI.
Hydroxyproline
Myofibroblast
Cardiac Fibrosis
Ventricular remodeling
Myocardial fibrosis
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Background:We evaluated 1 the sequential changes of angiotensin-converting enzyme (ACE mRNA expression in lung (main site for circulating ACE synthesis and left ventricle, and 2) whether such expression is modified by ACE inhibitor or angiotensin II receptor blocker treatment after acute myocardial infarction (MI in rats. Methods:Placebo, captopril (2 g/liter drinking water or TCV-116 (10 mg/kg/day gavage was administered 3 days before left coronary occlusion and continued for 6 weeks. At 1, 3 and 6 weeks after operation, hemodynamic measurement was performed and pulmonary and myocardial ACE mRNA expression was analyzed by quantitative RT-PCR using rcRNA as an internal standard. Results: Mean BP and LVEDP increased in untreated rats compared with captopril- and TCV-116-treated rats (post- MI 6week, p<0.05. Pulmonary ACE mRNA increased in acute phase (post-MI 1 week, max. 1.4 fold, p<0.05 vs. pre-MI and returned to pre-MI value thereafter. In contrast, cardiac ACE mRNA expression showed slightly decreasing tendency in acute phase, and was increased up to 1.6 fold in chronic phase after MI (post-MI 3 and 6weeks, p<0.05 vs. pre-MI. No changes in pulmonary ACE gene expression were found with RAS blockade. However, in acute phase after MI, cardiac ACE mRNA increased with both captopril and TCV-116 treatment (post-MI 24hour and 1week, max. 2 fold, p<0.05 vs. untreated group. Conclusion:1 In contrast to the pulmonary ACE mRNA that is activated in acute phase, the cardiac ACE mRNA is activated in chronic phase after MI. 2 RAS blockade does not affect the change of pulmonary
Peptidyl-Dipeptidase A
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To explore the potential role and mechanism of microRNA(miR)-30a in myocardial fibrosis after myocardial infarction (MI).Rats were randomly divided into 1 week MI group (n=11), 2 weeks MI group (n=13) and 4 weeks MI group (n=15) by applying random number table after left anterior descending coronary artery ligation. Rats in Sham group were examined at respective time points (n=16). Heart function was monitored by echocardiography. Myocardial collagen volume fraction (CVF) was determined on Masson stained sections. Myocardial expression of collagen Ⅰ and Ⅲ was determined by immunohistochemistry. The myocardial mRNA level of miR-30a, TGF-β1 and CTGF were detected by real time-quantitative PCR analysis. The myocardial protein levels of TGF-β1 and CTGF were measured by Western blot analysis.The LVEDD ((8.37±0.58) mm) and LVESD ((6.12±0.82) mm) in 4 weeks MI group were significantly higher than those in Sham group ((6.08±0.57) mm, (4.17±0.60) mm), all P<0.01. The FS ((27.0±3.9) %) and LVEF ((51.0±6.3) %) in 4 weeks MI group were significantly lower than those in Sham group ((47.0±2.1) %, (82.0±2.3)%), all P<0.01. The level of myocardial CVF in 1 week MI group, 2 weeks MI group and 4 weeks MI group were significantly higher than in Sham group (all P<0.01) in a time-dependent manner. The level of myocardial collagen Ⅰ and Ⅲ was increased gradually from 1 week to 4 weeks post MI compared with Sham group (all P<0.01). The collagen Ⅰ/Ⅲ ratio was similar between 1 week MI group and Sham group (P=0.58), however, which was significantly higher in 2 weeks MI group and 4 weeks MI group compared with Sham group (all P<0.01), and the ratio was significantly higher in 4 weeks MI group than 2 weeks MI group (P<0.01). The level of miR-30a was significantly and gradually reduced in all MI groups compared with Sham group (all P<0.01). The mRNA and protein levels of TGF-β1 and CTGF were significantly and gradually increased after MI compared with Sham group (all P<0.001).Our results indicate that overexpression of miR-30a after MI might be a potential strategy for suppressing myocardial fibrosis by modulating the mRNA and protein levels of TGF-β1 and CTGF.
Myocardial fibrosis
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Syndecan 1
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Hepatocyte growth factor (HGF) and vascular endothelial growth factor (VEGF) stimulate endothelial cell proliferation and induce angiogenesis, but the timing and significance of their release in patients with acute myocardial infarction (AMI) are unknown in relation to future left ventricular remodeling. Venous blood samples were obtained at admission and up to 3 weeks later in 40 patients with AMI and in 40 age- and sex-matched control subjects. Blood samples were also taken from the coronary sinus (CS) in 20 patients on day 7 following AMI. Left ventricular end-diastolic volume in the subacute (1 week) and chronic (3 months) phases was assessed by left ventriculography to identify the remodeling group (n=15), which was defined as an increase in left ventricular end-diastolic volume index > or =5 ml/m(2) relative to the baseline value. Serum HGF and VEGF concentrations were higher in newly admitted patients with AMI than in the controls (HGF, 0.33 +/-0.09 vs 0.24+/-0.08 ng/ml, p<0.01; VEGF, 92.2+/-43.1 vs 67.2+/-29.8 pg/ml, p<0.01), peaking on day 7 (HGF, 0.41+/-0.12; VEGF, 161.7+/-76.9), and gradually decreasing between days 14 and 21. The HGF concentration in the CS did not differ from the concentration in the periphery, but the VEGF concentration was significantly more abundant in the CS than in the peripheral sample on day 7 (p<0.05). The serum HGF concentration on day 7 was higher in the remodeling group than in the nonremodeling group (0.47 +/-0.13 vs 0.36+/-0.09 ng/ml, p<0.01), but there was no difference between the groups on admission, day 14 and day 21. The serum VEGF concentration did not differ between the remodeling and nonremodeling groups at any time. Thus, the serum HGF concentration on day 7 after AMI is mostly from noncardiac sources and predicts left ventricular remodeling.
Ventricular remodeling
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AimsControversy exists regarding the effects of granulocyte colony-stimulating factor (G-CSF) on post-infarction remodelling, which is regulated by matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs). The aim of this study was to investigate the impact of G-CSF administration on cardiac MMP/TIMP ratios and long-term remodelling in a rat model of acute myocardial infarction (MI).
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