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Transcription profiling of mouse - effect of PGF receptor FP on bleomycin-induced pulmonary fibrosis

ABSTRACT: We purposed to examine the effect of PGF receptor FP in development of ; bleomycin-induced pulmonary fibrosis in mice. We performed gene ; expression analysis in the lung of WT and FP-KO mice on Days 0, 7 and ; 14. We found out that fibrosis-related genes such as various isoforms ; of collagen, which were induced on Day 7 and continued to increase or ; remained unchanged on Day 14, were induced to less extent in FP-KO ; mice. In contrast, expression of inflammation-related genes peaked on ; Day 7 similarly in WT and FP-KO mice. These results suggest that FP ; functions in fibrosis-phase, not in peak inflammation phase, and ; facilitates fibrogenesis by enhancing expression of fibrosis-related ; genes. Experiment Overall Design: RNA was prepared from the lung of WT and FP-KO mice on Day 0, 7 and 14 Experiment Overall Design: (n=4-5 for each group at each time point) after bleomycin instillation, Experiment Overall Design: and used for hybridization with Affymetrics mouse 430 2.0 microarrays. Experiment Overall Design: Time-dependent changes in expression of genes in FP-KO mice were Experiment Overall Design: compared with those in WT mice.

ORGANISM(S): Mus musculus

SUBMITTER: Sakata Daiji

PROVIDER: E-GEOD-18800 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Effect of PGF receptor FP on bleomycin-induced pulmonary fibrosis in mice

Project description:We purposed to examine the effect of PGF receptor FP in development of bleomycin-induced pulmonary fibrosis in mice. We performed gene expression analysis in the lung of WT and FP-KO mice on Days 0, 7 and 14. We found out that fibrosis-related genes such as various isoforms of collagen, which were induced on Day 7 and continued to increase or remained unchanged on Day 14, were induced to less extent in FP-KO mice. In contrast, expression of inflammation-related genes peaked on Day 7 similarly in WT and FP-KO mice. These results suggest that FP functions in fibrosis-phase, not in peak inflammation phase, and facilitates fibrogenesis by enhancing expression of fibrosis-related genes.

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