Modulation of actin isoform expression in alveolar myofibroblasts (contractile interstitial cells) during pulmonary hypertension.

摘要: Lungs of 37 patients with pulmonary hypertension (PHT), 5 normal human lungs, and 30 rat were studied using immunohistochemical stainings for actin, alpha-smooth muscle (alpha-SM) actin desmin. The type PHT was determined on clinicopathologic grounds (in 17 cases by catheterism); 20 had precapillary postcapillary PHT. In myofibroblasts, ie, contractile interstitial cells (CIC), distributed in alveolar septa, not stained alpha-SM antibodies. Only around the venules, labeled this antibody present. Furthermore, there bundles actin-positive openings air sacculi into ducts. PHT, distribution immunostaining properties remained unchanged; observed thickened arterial intima plexiform lesions. secondary to heart failure, mitral stenosis, or veno-occlusive disease, many septa decorated antibodies but authors propose that, mechanical stretch due capillary congestion may be responsible generation that express an isoform associated smooth muscle.