Emphysema, a pathological component of chronic obstructive pulmonary disease, causes irreversible damage to the lung. Previous studies have shown that Slit plays essential roles in cell proliferation, angiogenesis, and organ development. In this study, we evaluated the effect of Slit2 on the proliferation and migration of mouse lung epithelial cells and its role in regeneration in an emphysema lung mouse model. Here, we have shown that Slit2/Robo signaling contributes to the regeneration of lungs damaged by emphysema. Mouse epithelial lung cells treated with Slit2 exhibited increased proliferation and migration in vitro. Our results also showed that Slit2 administration improved alveolar regeneration in the emphysema mouse model in vivo. Furthermore, Slit2/Robo signaling increased the phosphorylation of ERK and Akt, which was mediated by Ras activity. These Slit2-mediated cellular signaling processes may be involved in the proliferation and migration of mouse lung epithelial cells and are also associated with the potential mechanism of lung regeneration. Our findings suggest that Slit2 administration may be beneficial for alveolar regeneration in lungs damaged by emphysema.

肺气肿是慢性阻塞性肺病的病理组成部分，会对肺造成不可逆的损害。先前的研究表明，狭缝在细胞增殖、血管生成和器官发育中起着重要作用。在本研究中，我们评估了 Slit2 对小鼠肺上皮细胞增殖和迁移的影响及其在肺气肿肺小鼠模型中的再生作用。在这里，我们已经证明 Slit2/Robo 信号有助于肺气肿损伤的肺的再生。用 Slit2 处理的小鼠肺上皮细胞在体外表现出增加的增殖和迁移。我们的研究结果还表明，在体内肺气肿小鼠模型中，Slit2 给药改善了肺泡再生。此外，Slit2/Robo 信号增加了 ERK 和 Akt 的磷酸化，这是由 Ras 活性介导的。这些 Slit2 介导的细胞信号传导过程可能参与了小鼠肺上皮细胞的增殖和迁移，也与肺再生的潜在机制有关。我们的研究结果表明，Slit2 给药可能有利于肺气肿损伤的肺泡再生。