Fig. 4

Upregulation of GAB1 ameliorates BPD in neonatal mice. A&B, Western blot analysis of GAB1 protein in lung tissues of each group. ^* p < 0.05 vs. neonatal mice under RA exposure (the RA group). ^# p < 0.05 vs. neonatal mice with hyperoxia-induced BPD receiving oe-NC vector injection (the BPD + oe-NC group). ^& p < 0.05 vs. neonatal mice with hyperoxia-induced BPD receiving antagomir-NC injection (the BPD + antagomir-NC group). C, HE staining analysis of lung tissues in each group (× 400). D, Alveolar chord length of lung tissues in each group. E&F, Positive expression level of Ki67 in lung tissues of each group determined by immunohistochemistry (× 400). G&H, Cell apoptosis in lung tissues of each group assessed by TUNEL staining (× 200). I&J, Western blot analysis of apoptosis-related proteins (Bax, Caspase-3 and Bcl-2) in lung tissues of each group. K&L, Positive expression rate of CD31 protein in lung tissues of each group determined by immunohistochemistry (× 400). In panel C-L, ^* p < 0.05 vs. neonatal mice with hyperoxia-induced BPD receiving oe-NC vector injection (the BPD + oe-NC group). ^# p < 0.05 vs. neonatal mice with hyperoxia-induced BPD receiving an injection of antagomir-NC combined with oe-NC vector (the BPD + antagomir-NC + oe-NC group). N = 15. Measurement data were expressed as mean ± standard error. Data comparison between two groups was examined by unpaired t-test. miR-29a, microRNA-29a; GAB1, GRB2-associated-binding protein 1; BPD, bronchopulmonary dysplasia; RA, room air; Bax, Bcl-2-associated X protein; Bcl-2, B-cell lymphoma 2; HE, hematoxylin-eosin; RAC, radial alveolar counts; TUNEL, TdT-mediated dUTP-biotin nick end-labeling; NC, negative control