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- W1634403590 abstract "IPF is a chronic disease with high lethality rate due to factors such as poor prognosis, unknown etiology and limited response to current therapies. Fibroblast activation and proliferation and ECM deposition are hallmarks of IPF leading to abnormal lung architecture and loss of respiratory function. Coactivator-associated arginine methylatransferase 1 (CARM1), an arginine methyltransferase and transcriptional cofactor, is important for lung development as a regulator of pulmonary epithelial cell proliferation and differentiation. We therefore investigate its role in the development of IPF. To induce fibrosis C57BL/6 wild type (wt) and CARM1 +/- mice were instilled with 3U/kg of bleomycin or a PBS control. Lung function, histology and gene expression were analysed. Bleomycin instillation resulted in reduced compliance after 7 days for both wt & Carm1 -/+ mice (PBS vs bleomycin, wt: 0.039±0.002 vs 0.030±0.002, Carm1 -/+ : 0.045±0.002 vs 0.035±0.003, mean ± s.e.m., ml/cmH 2 O). Interestingly after 21 days lung function had improved in the wt mice (0.035±0.001 vs 0.031±0.002) but not in the Carm1 +/- mice (0.042±0.002 vs 0.031±0.002 pl0.05). Furthermore, H&E staining revealed characteristic fibrosis in the wt mice that peaked at days 21 and 28 before resolving. However, fibrosis remained high at d35 in the CARM1 +/- mice with an Ashcroft score of 2.7±0.5 compared to 1.1±0.3 (mean ± s.e.m.) in the wt mice. Furthermore, our gene expression analysis revealed a 2-fold increase of Pai-1 and β-catenin mRNA levels in the CARM1 +/- mice compared to wild types, both important mediators of pulmonary fibrosis. In summary, reduction of CARM1 prolongs bleomycin-induced pulmonary fibrosis, suggesting a potential future therapeutic intervention." @default.
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- W1634403590 date "2014-09-01" @default.
- W1634403590 modified "2023-09-28" @default.
- W1634403590 title "Loss of CARM1 prolongs bleomycin-induced pulmonary fibrosis" @default.
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