Journal
SCIENTIFIC REPORTS
Volume 6, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/srep18946
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Funding
- Special Funds for Major State Basic Research Projects [2012CB518104]
- National Natural Science Foundation of China [81170059]
- NINDS [K02NS081000]
- Specialized Research Fund for the Doctoral Program of Higher Education of China [20130162110052]
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Triggering receptor expressed on myeloid cells 1 (TREM-1) increases the expression of TGF-beta family genes, which are known as profibrogenic cytokines in the pathogenesis of pulmonary fibrosis. In this study, we determined whether TGF-beta 1 regulated the expression of TREM-1 in a mouse model of pulmonary fibrosis. The expression of TGF-beta 1 and TREM-1 was increased on day 7, 14, and 21 after single intratracheal injection of bleomycin (BLM). And there was positive correlation between the expression of TGF-beta 1 and TREM-1. TGF-beta 1 increased expression of TREM-1 mRNA and protein in a time-and dose-dependent manner in mouse macrophages. The expression of the activator protein 1 (AP-1) was increased in lung tissues from mouse after BLM injection and in mouse macrophages after TGF-beta 1 treatment, respectively. TGF-beta 1 significantly increased the relative activity of luciferase in the cells transfected with plasmid contenting wild type-promoter of TREM-1. But TGF-beta 1 had no effect on the activity of luciferase in the cells transfected with a mutant-TREM1 plasmid carrying mutations in the AP-1 promoter binding site. In conclusion, we found the expression of TREM-1 was increased in lung tissues from mice with pulmonary fibrosis. TGF-beta 1 increased the expression of TREM-1 in mouse macrophages partly via the transcription factor AP-1.
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