Article
Interaction of H2O2 and TGF-beta1 in an in-vitro wound model of respiratory epithelial cells
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Published: | March 26, 2015 |
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Introduction: Human airway epithelium acts as a protective barrier and is subject to injury during exposure to a variety of inhaled toxins or infectious agents, such as reactive oxygen species (ROS). Repair of epithelial injury requires a wound repair process, in which TGF-beta1 exerts an important function. However stimulating efficacy and the interaction between ROS and TGF-beta1 in airway wound healing remain not clearly described.
Methods: Two kinds of airway epithelial cells, S9 and A549, were treated with hydrogen peroxide (H2O2) and /or TGF-beta1 and with/without corresponding inhibitors (catalase, SB431542). An in vitro wound model was used to figure out the effect on wound healing; the number of living cells was measured by CASY; the morphology of cells was analyzed by microscopy; intracellular ROS changes were identified by 2-Cys Prx Redoxblot; the TGF-beta1 level in supernatants was tested by ELISA.
Results: Cell growth was inhibited by H2O2 in a time and dose-dependent manner in both S9 and A549 cell lines. TGF-beta1 induced S9 epithelial cell growth during the first 24 hours, but inhibited cell growth after 72 hours. In contrast A549 cells growth was time-dependently inhibited. TGF-beta1 also induced morphologic changes of S9 cells into a spindly shape. Both H2O2 and TGF-beta1 affected the wound healing capacity significantly and TGF-beta1 expression and level of ROS were affected in S9 and A549 epithelial cell lines.
Conclusions: ROS and TGF-beta1 show cellular interactions in airway epithelial cell growth and wound healing.
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