Cell and Molecular Mediators involved in damage and repair in emphysema using mouse models

摘要: Chronic obstructive pulmonary disease (COPD) is the third leading cause of morbidity and mortality in United States an epidemic worldwide. COPD pathologically manifests as emphysema, which characterized by abnormal permanent airspace enlargement. Current research strives to understand exact sequence events triggering progression this disease, with continued hope finding a cure. The overarching aim current study was investigate role for receptor advanced glycation end products (RAGE) distal bronchial progenitor cell population (DBPCs) mediating alveolar damage repair using murine models emphysema. RAGE has gained importance context past decade. Highly expressed normal adult lung tissue; its expression altered injury. present tests hypothesis that RAGE mediates cigarette smoke induced injury based on previously described pro-inflammatory function. knockout mice (RAGE-/-) were used contribution towards development emphysema. Our data indicates RAGE’s key mediated through neutrophil recruitment increased loss tissue elastance. Emphysema thought result from disruption delicate balance exists within compartment; accentuated failure at endogenous attempts presence extensive inflammation underlying basement membrane. Using transgenic mouse line (CC10-Cre x Rosa26-LacZ) developed our laboratory, we trace confirm migration bronchoalveolar duct junction (BADJ)/ terminal bronchioles into adjacent injured compartment. We further findings knock-in (CC10-iCre X thereby authenticate these cells repopulating alveolus. This shows early pathogenic elucidates CC10 expressing arising airways repopulation