Abstract
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.
Highlights
Pulmonary hypertension due to left heart disease (PH-LHD) belongs to type II pulmonary hypertension (PH) and is the most common type of PH in clinical practice [1, 2]
We revealed that stretch-activated channel (SAC)/mitogen-activated protein kinases (MAPKs) signaling pathway could be involved in the upregulations of matrix metalloproteinase-9 (MMP-9) and transforming growth factor-β1 (TGF-β1) mediated by mechanical stretching in pulmonary vein
Right ventricular systolic pressure (RVSP) and mean left atrial pressure (mLAP) were determined in PH-LHD model rats
Summary
Pulmonary hypertension due to left heart disease (PH-LHD) belongs to type II pulmonary hypertension (PH) and is the most common type of PH in clinical practice [1, 2]. It is usually initiated by left ventricular dysfunction, which results in increased left ventricular end-diastolic pressure, increased left atrial pressure, and increased pulmonary venous pressure. This eventually leads to PH and pulmonary artery revascularization [1, 3]. Whether pulmonary venous hypertension in the early stage of the disease participates in pulmonary artery remodeling has not been reported
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