Journal
RESPIRATORY RESEARCH
Volume 23, Issue 1, Pages -Publisher
BMC
DOI: 10.1186/s12931-022-02027-4
Keywords
PEDF; IPF; Bleomycin; Fibroblast; PPAR-gamma
Categories
Funding
- National Natural Science Foundation of China [81870235, 81400227, 81570242]
- Social Development Projects of Key R&D Programs in Jiangsu Province [BE2019643]
- National Natural Science Foundation of Jiangsu Province [BK20171178]
- General Program of Jiangsu Commission of Health [H2017083]
- Project of Invigorating Health Care through Science, Technology and Education, Jiangsu Provincial Medical Youth Talent [QNRC2016778]
- Foundation of Jiangsu Province Six Talents Peak [2015-WSN-063]
- Postgraduate Research & Practice Innovation Program of Jiangsu Province [KYCX21_2683, KYCX21_2687]
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This study demonstrates that PEDF can act as an anti-fibrotic factor, inhibiting fibroblast activation by upregulating PPAR-gamma activity and reducing bleomycin-induced pulmonary fibrosis in rats.
Background: Idiopathic pulmonary fibrosis (IPF) is a highly heterogeneous and fatal lung disease. In addition to dense fibrous tissue, abnormal angiogenesis is also an important feature of IPF. Pigment epithelium-derived factor (PEDF) is an angiogenesis inhibitor and a potential anti-fibrous factor. The purpose of this experiment is to observe the effect of PEDF on bleomycin (BLM)-induced pulmonary fibrosis in rats. Methods: In vivo, pathological examination and detection of related factors were performed on pulmonary fibrosis induced by BLM in rats, and the temporal and spatial distribution of PEDF was investigated. Furthermore, lung gene delivery (PEDF-adeno-associated virus) was performed to investigate the effect of PEDF on pulmonary fibrosis. In vitro, lentiviral vectors were used to construct PEDF over-expression or knock out primary rat lung (PRL) fibroblasts. The effect of PEDF on fibroblast activation under TGF-beta 1 stimulation was evaluated, and the activation of TGF-beta 1/smad pathway and PPAR-gamma expression (in the presence or absence of PPAR-gamma inhibitors) were analyzed. Results: In vivo results showed that PEDF expression decreased during the inflammatory phase and increased during the fibrotic phase. PEDF could inhibit the progression of pulmonary fibrosis in rats. In vitro results showed that PEDF could effectively inhibit TGF-beta 1-stimulated fibroblast activation and reduce the production of alpha-SMA and collagen-I. PEDF could inhibit the TGF-beta 1/smad pathway by up-regulating the activity of PPAR-gamma. Conclusions: PEDF can act as an anti-fibrotic factor, inhibit fibroblast activation by upregulating PPAR-gamma activity and reduce BLM-induced pulmonary fibrosis in rats.
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