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首页> 外文期刊>PLoS One >Mechanical stretching of pulmonary vein stimulates matrix metalloproteinase-9 and transforming growth factor-β1 through stretch-activated channel/MAPK pathways in pulmonary hypertension due to left heart disease model rats
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Mechanical stretching of pulmonary vein stimulates matrix metalloproteinase-9 and transforming growth factor-β1 through stretch-activated channel/MAPK pathways in pulmonary hypertension due to left heart disease model rats

机译：肺静脉的机械拉伸刺激基质金属蛋白酶-9，通过左心疾病模型大鼠引起肺动脉高压的拉伸活化通道/ MAPK途径转化生长因子-β1

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Pulmonary hypertension due to left heart disease (PH-LHD) is a momentous pulmonary hypertension disease, and left heart disease is the most familiar cause. Mechanical stretching may be a crucial cause of vascular remodeling. While, the underlining mechanism of mechanical stretching-induced in remodeling of pulmonary vein in the early stage of PH-LHD has not been completely elucidated. In our study, the PH-LHD model rats were successfully constructed. After 25 days, doppler echocardiography and hemodynamic examination were performed. In addition, after treatment, the levels of matrix metalloproteinase-9 (MMP-9) and transforming growth factor-β1 (TGF-β1) were determined by ELISA, immunohistochemistry and western blot assays in the pulmonary veins. Moreover, the pathological change of pulmonary tissues was evaluated by H&E staining. Our results uncovered that left ventricular insufficiency and interventricular septal shift could be observed in PH-LHD model rats, and the right ventricular systolic pressure (RVSP) and mean left atrial pressure (mLAP) were also elevated in PH-LHD model rats. Meanwhile, we found that MMP-9 and TGF-β1 could be highly expressed in PH-LHD model rats. Besides, we revealed that stretch-activated channel (SAC)/mitogen-activated protein kinases (MAPKs) signaling pathway could be involved in the upregulations of MMP-9 and TGF-β1 mediated by mechanical stretching in pulmonary vein. Therefore, current research revealed that mechanical stretching induced the increasing expressions of MMP-9 and TGF-β1 in pulmonary vein, which could be mediated by activation of SAC/MAPKs signaling pathway in the early stage of PH-LHD.
机译：由于左心疾病（pH-LHD）引起的肺动脉高压是一种重大的肺动脉高压疾病，左心疾病是最熟悉的原因。机械拉伸可能是血管重塑的关键原因。虽然，在pH-LHD早期的肺静脉中重塑的机械拉伸诱导的强调机制尚未完全阐明。在我们的研究中，PH-LHD模型大鼠成功构建。 25天后，进行多普勒超声心动图和血液动力学检查。另外，在治疗后，基质金属蛋白酶-9（MMP-9）和转化生长因子-β1（TGF-β1）的水平由ELISA，免疫组化和肺静脉中的蛋白质印迹测定法测定。此外，通过H＆E染色评估肺组织的病理变化。我们的结果发现，在pH-LHD模型大鼠中可以观察到左心室不足和间隔偏移，并且在pH-LHD模型大鼠中也升高了右心室收缩压（RVSP）和平均左心房压（MLAP）。同时，我们发现MMP-9和TGF-β1可以在pH-LHD模型大鼠中高度表达。此外，我们揭示了拉伸激活的通道（SAC）/丝肠激活蛋白激酶（MAPK）信号传导途径可以参与由肺静脉中机械拉伸介导的MMP-9和TGF-β1的上调。因此，目前的研究表明，机械拉伸诱导肺静脉中MMP-9和TGF-β1的增加表达，这可以通过PH-LHD的早期激活SAC / MAPKS信号通路的激活来介导。

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