Abstract
Background: Pulmonary emphysema is a chronic lung disease marked by destruction of the lung's gas-exchange structures and is so far irreversible. Recently, it has been reported that an exogenous rHuKGF has the potential to induce alveolar epithelium proliferation in emphysematous lungs of mice. Objective: The aim of the present study was to investigate the effect of rHuKGF in the lungs of emphysema challenged mice on MAPK/ERK mediated signalling pathway that regulates alveolar epithelial cell proliferation. Methods: Three experimental groups [i.e., emphysema (ES), therapy model for emphysema (EK) and control (SS)] were prepared. Subsequently, lungs from each mouse were collected for histopathology & QPCR based analyses. Results: Histopathology-based photomicrographs clearly represented that the rHuKGF treated emphysematous lungs reversed the loss of alveolar septa, which were lost in elastase treated lungs compared to healthy lungs. Upon validation on molecular level, QPCR studies revealed that the mRNA levels of FGF7, FGFR2, Ras, c-Raf, Erk1, Erk2, c-Myc and CREBBP were significantly increased while Elk-1 was notably decreased in therapy group when compared with emphysema group and were well comparable with the control group. Conclusion: Therapeutic supplementation of rHuKGF ameliorates the deregulated MAPK/ERK pathway in emphysema condition, resulting in alveolar epithelium regeneration. Hence rHuKGF may prove to be a potential drug in the treatment of emphysema; however, further elaborated studies are to be conducted.
- © 2013 ERS
