Hepatic differentiation in the lungs of Mgp^−/− mice. (a) Gene expression profiles from lungs and liver of WT (Mgp^+/+) and Mgp^−/− mice (n = 2). (b) Genes involved in liver metabolism with extraction of significant difference in expression (P < 0.05). (c and d) Expression of select hepatic markers was analyzed by real-time PCR. The difference in expression was calculated as a fold change as compared between Mgp^+/+ and Mgp^−/− lungs (n = 10). (e and f) Albumin levels (e) and activity of P450 (f) were compared in cells isolated from Mgp^+/+ and Mgp^−/− lungs. Isolated hepatocytes from Mgp^+/+ and Mgp^−/− liver were used as controls (n = 8). (g) Schematic diagram of strategy for detecting albumin promoter–driven expression of β-galactosidase (LacZ) in the lungs of Mgp^−/− mice. (h) 5-bromo-4-chloro-3-indolyl-β-d-galactopyranoside (X-gak) staining of lungs of Alb^CreRosa^LacZMgp^+/+ and Alb^CreRosa^LaczMgp^−/− mice (n = 3). (i) Schematic diagram of strategy for detecting albumin promoter–driven expression of EGFP in the lungs of Mgp^−/− mice. (j) EGFP-positive cell populations in cells isolated from lungs of Alb^CreRosa^eGfpMgp^+/+ and Alb^CreRosa^EGFPMgp^−/− mice were assessed by flow cytometric analysis (n = 3). (k) Pulmonary function of Mgp^−/− mice (n = 4). CO₂, hypercapnia phase with 7% CO₂, 21% O₂, and balanced N₂. RA, room air. (l) Expression of pulmonary markers in lungs of Mgp^−/− mice. Mgp^+/+ lung was used as control (n = 6). (m) Expression of albumin in lungs, artery, brain, kidneys, bone, heart, muscle, and liver in Mgp^−/− mice. Mgp^+/+ was used as control (n = 6). Data in c–f and k–m were analyzed by two-sided t test. **, P <0.005; ***, P < 0.001. Error bars are standard deviation. Data distribution was assumed to be normal, but this was not formally tested. Bars, 1 mm.