| Pulmonary hypertension is a common complication of cardiopulmonary diseases. Regardless of the etiology, all patients with chronic pulmonary hypertension have structural pulmonary vascular changes, right ventricular hypertrophy and, in the long term, right ventricular failure. Changes in the pulmonary vasculature that accompany with elevations in pulmonary vascular pressure are generally referred to as pulmonary vascular remodeling.Pulmonary vascular remodelling is an important pathological feature of pulmonary hypertension, associated with abnormal endomelial morphology and function, muscularization of normally nonmuscular peripheral arteries related to differentiation of pericytes or/and vascular smooth muscle cell, and medial hypertrophy and neointimal formation in muscular arteries, leading to increased pulmonary vascular resistance and reduced compliance. Pulmonary vascular remodeling involves structural changes in the normal architecture of the walls of pulmonary arteries as a consequence of hypertrophy, proliferation, and migration of the predominant cell type within each layer, as well as increased production of extracellular matrix (ECM) components.Tenascin-C ( TN-C ), being absent or scantily expressed in most adult tissues, is an oligometric glycoprotein of the extracellular matrix that is prominent during normal and pathological tissue restructuring, including embryonic development, epithelialmesenchymal interactions, wound healing, and cancer, where it is believed to modulate morphogenetic events including cell migration and proliferation. In addition, TN-C may regulate endothelial and SMC behavior directly through interactions with a myriad of cell surface receptors, which transduce extracellular information to the intracellular machinery that controls cell growth, differentiation. Previous studies have documented that, in cardiovascular tissues, TN-C expressed in carotid arteries afterexperimental balloon injury and has recently been linked to cell proliferation in neointimal lesions in polytetrafluoroethylene grafts.In this study, the development of vascular changes in MCT-treated rats is likely initiated by endothelial cell injury is reported. By immunohistochemistry staining combined with light microscopy that increased TN-C expression accompanies progressive vascular changes were observed in MCT-treated rats. In parallel studies, western blot analyses was used to show that induction and increased deposition of TN-C protein correlated with increased steady state levels of TN-C mRNA by reverse transcription-polymerase chain reaction ( RT-PCR ) within intrapulmonary vessels.Part one: Pulmonary Artery Remodeling inMonocrotaline-induced Pulmonary Hypertensive RatsObjective Pulmonary arterial hypertension is a common complication of cardiopulmonary diseases, Regardless of the etiology, chronic pulmonary hypertension is characterized by pulmonary vascular remodeling secondary to a abnormal proliferation of vascular endothelial and smooth muscle cells as well as extra extracellular matrix deposition. To analyzed structural characteristics of muscular pulmonary arteries and arterioles in classic model of pulmonary hypertensive rat induced by monocrotaline and its relationship with pulmonary hypertension, to examine quantitatively the remodeling of intra-acinar blood arteries in hypentensive rat lungs.Methods Seventy-two Sprague-Dawley rats were randomly assigned into the control (CON) group and monocrotaline (MCT) group. MCT was subcutaneously administrated by a single injection into male rats. The mean of pulmonary arterial pressure (mPAP) was measured directly by right-heart catheterization, respectively. The ratio of the right ventricleweight (RV) to left ventricle weight (LV) plus septum weight (S) [RV/(LV+S)] were measured and calculated as right ventricular hypertrophy index (RVHI). The lumen area and the media cross-sectional area of pulmonary arteries with an external diameter between 30 ~ 100 micrometer and 101 ~ 200 micrometer were analysised by light microscopy, the num... |
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