Abstract
BackgroundOrgan regeneration in mammals is hypothesized to require a functional pool of stem or progenitor cells, but the role of these cells in lung regeneration is unknown.MethodsBased on the fact that postnatal regeneration of alveolar tissue has been attributed to alveolar epithelial cells, we established a hemorrhagic shock and Lipopolysaccharide (LPS) lung injury model. Using this model, we analyzed the cellular kinetics of lung alveolar epithelial cells.ResultsThe results showed that alveolar epithelium type 2 cells (AEC2s) are damage resistant during acute lung injury, they might be the main cells involved in lung injury and repair. Then we observed the relationship between the expression of HGF, c-Met following ALI in rat lung and proliferation of AEC2s. The proliferation of AEC2s was inhibited when isolated primary AEC2s were co-cultured with c-Met inhibitor SU11274. Furthermore, the numbers of AEC2s was significantly decreased when ALI rats were administrated with SU11274 in vivo. It provided further evidence that the HGF/c-Met signaling plays a vital role in ALI-induced AEC2s proliferation.ConclusionsAEC2s are damage resistant during acute lung injury and the HGF/c-Met signaling pathway is of vital importance in the proliferation of AEC2s after ALI.
Highlights
Organ regeneration in mammals is hypothesized to require a functional pool of stem or progenitor cells, but the role of these cells in lung regeneration is unknown
In terms of mechanism research, we explored the role of Hepatocyte Growth Factor (HGF)/c-Met signaling pathway in Type 2 alveolar epithelial cells (AEC2) proliferation after Acute lung injury (ALI)
Kinetics of alveolar epithelial cells after acute lung injury Acute lung injury model Rat hemorrhagic shock and LPS lung injury model was established, we found that rats exposed to 4.0 mg/kg LPS instilled intratracheally exhibited 100% survival, the area of pulmonary hemorrhage is only about 5%–10%
Summary
Organ regeneration in mammals is hypothesized to require a functional pool of stem or progenitor cells, but the role of these cells in lung regeneration is unknown. When the epithelial cells lining the interior of the lung are damaged by infection with influenza virus, a rare stem-cell population distal airway stem cells (DASCs) is induced to proliferate and migrate to the damaged site. They can differentiate into alveolar epithelium type 1 and type 2 cells (AEC1/2 s) [4]. AEC2s are widely accepted as progenitor cells of lung and contribute to the lung repair and regeneration process. AEC1s and AEC2s arise from a bipotent progenitor cell lineage, whereas after
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