Gene expression data from type II pneumocytes from adult mice with and without Trf2

ABSTRACT: Gas exchange in the mammalian lung occurs in the alveolar sacs lined by epithelial cells that form a barrier allowing effective oxygen diffusion. Telomere syndromes have their most common manifestation in degenerative disease of the alveoli, both pulmonary fibrosis and emphysema. We tested the role of telomere dysfunction by inducing deletion of the telomere binding protein Trf2 in type 2 alveolar epithelial cells (AEC2s) that both express the gene encoding surfactant protein C and constitute the regenerative compartment of the alveolar epithelium. Acquired telomere dysfunction in these cells preferentially induced cellular senescence, and mouse lungs were marked by an inflammatory response even though the telomere dysfunction was restricted to the epithelium. Senescent AECs had alter

ORGANISM(S): Mus musculus

SUBMITTER: Mary Armanios 

PROVIDER: E-GEOD-56892 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress