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. 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.
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.
Project description:Bleomycin-induced pulmonary fibrosis in mice mimics major hallmarks of idiopathic pulmonary fibrosis, yet in this model it spontaneously resolves over time. We studied molecular mechanisms of fibrosis resolution and lung repair, focusing on transcriptional and proteomic signatures and the effect of aging. Young (3 months) and old (21 months) mice were treated with Bleomycin or with control saline solution and analyzed transcript and protein expression over 8 weeks (Day 0, 14, 21, 28, 35, 42, 49, 56).
Project description:Bleomycin-induced pulmonary fibrosis in mice mimics major hallmarks of idiopathic pulmonary fibrosis, yet in this model it spontaneously resolves over time. We studied molecular mechanisms of fibrosis resolution and lung repair, focusing on transcriptional and proteomic signatures and the effect of aging. Young (3 months) and old (21 months) mice were treated with Bleomycin or with control saline solution and analyzed transcript and protein expression over 8 weeks (Day 0, 14, 21, 28, 35, 42, 49, 56).
Project description:Bleomycin-induced pulmonary fibrosis in mice mimics major hallmarks of idiopathic pulmonary fibrosis, yet in this model it spontaneously resolves over time. We studied molecular mechanisms of fibrosis resolution and lung repair, focusing on transcriptional and proteomic signatures and the effect of aging. Old mice showed delayed and incomplete lung function recovery 8 weeks after Bleomycin instillation. This shift in structural and functional repair in old Bleomycin-treated mice was reflected in a temporal shift in gene and protein expression. We reveal gene signatures and signaling pathways which underpin the lung repair process.