Transcription repressor Bach2 is required for pulmonary surfactant homeostasis and alveolar macrophage function.

ABSTRACT: Pulmonary alveolar proteinosis (PAP) results from a dysfunction of alveolar macrophages (AMs), chiefly due to disruptions in the signaling of granulocyte macrophage colony-stimulating factor (GM-CSF). We found that mice deficient for the B lymphoid transcription repressor BTB and CNC homology 2 (Bach2) developed PAP-like accumulation of surfactant proteins in the lungs. Bach2 was expressed in AMs, and Bach2-deficient AMs showed alterations in lipid handling in comparison with wild-type (WT) cells. Although Bach2-deficient AMs showed a normal expression of the genes involved in the GM-CSF signaling, they showed an altered expression of the genes involved in chemotaxis, lipid metabolism, and alternative M2 macrophage activation with increased expression of Ym1 and arginase-1, and the M2 regu

ORGANISM(S): Mus musculus

SUBMITTER: ari itoh 

PROVIDER: E-GEOD-54050 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress