Fig. 6
From: SOX9 inactivation affects the proliferation and differentiation of human lung organoids
SOX9−/− does not affect the differentiation of alveolar cells or their role in promoting the functional recovery of injured mice. A Schematic of the experimental design. B–D Immunofluorescence labeling of human mitochondria marker MAB1273, AT2 marker pro–SP-C, AT1 marker human PDPN (HU-PDPN), and distal progenitor marker SOX9 in transplanted SOX9 wild-type (WT) and knockout (SOX9−/−) lung progenitor organoids. White arrowhead in B indicates cells coexpressing MAB1273 and pro–SP-C; white arrowhead in C indicates cells coexpressing HU-PDPN and pro–SP-C. n = 4 (WT), n = 5 (SOX9-/-). Scale bars, 100 μm (B, left panels of each sample); 50 μm (B, right panels of each sample; C; D). E Hematoxylin and eosin (H&E) and Masson’s trichrome staining of transplanted WT and SOX9−/− lung progenitor organoids. Scale bars, 500 μm (top); 100 μm (bottom). F Arterial blood gas analysis. Partial oxygen pressure (pO2), partial carbon dioxide pressure (pCO2), and oxygen saturation (sO2) were measured in WT and SOX9−/− organoid-transplanted mice. Data represent mean ± SEM (n = 3)