Page 61 - F. Cell biology

Blockade of CSF3 can reverse lung fibrosis in bleomycin model

In-Yeong Yun¹, Jae-Hyeok Kang¹, Mi-Young Choi¹, Min-Jung Kim², Su-Jae Lee¹
Department of Life Science, Research Institute for Natural Sciences, Hanyang University, Seoul 04763, Korea

Background AIM
Idiopathic pulmonary fibrosis (IPF) is a progressive interstitial IPF-specific therapies still have not been developed, and early
lung disease characterized by worsening lung function with recognition, accurate diagnosis and effective treatment for IPF
dyspnea. The main symptoms of patients suffering from IPF are urgently needed. The aim of this study was to evaluate CSF3
include fatigue, unexpected weight loss and dry cough. There is no as a potential therapeutic target of IPF and define its molecular
evidence of continuous stimuli, but risk factors include smoking, mechanism.
age, and generic factors. The average survival rate of the diagnosed
patients is reported within approximately 3 years.
Methods

Bleomycin (BLM) induced mouse IPF model, immunohistochemistry, RT-qPCR and western blot were used to demonstrate the
regulatory mechanisms of CSF3.
The microarray data of IPF Patients were analyzed by gene set enrichment analysis (GSEA).

Results

Figure 1. BLM induced EMT promotes trans-differentiation Figure 3. Neutralization of CSF3 accelerates resolution
of lung epithelial cells to myofibroblasts BLM-induced lung fibrosis

Figure 2. CSF3 mediates EMT of lung epithelial cells and Figure 4. Pretreatment of CSF3 ab can prevent lung fibrogenesis
upregulated in lung fibrosis model in mouse IPF model

Conclusion References Contact Information

Collectively, our results demonstrated 1. Rangarajan, S., et al. Metformin reverses In-Yeong Yun
that CSF3 is a major regulator of IPF established lung fibrosis in a bleomycin Laboratory of Molecular Biochemistry,
Department of Life Science, Hanyang
through EMT of lung epithelial cells and model. Nat Med 24, 1121-1127 (2018). University, 222, Seoul 04763 Korea.
blockade of CSF3 may reverse the 2. Anathy, V., et al. Reducing protein E-mail: mydlsdud@naver.com
fibrosis by facilitating deactivation of oxidation reverses lung fibrosis. Nat Med 24,
1128-1135 (2018).
myofibroblasts and suggests that CSF3 3. Barratt, S.L., Creamer, A., Hayton, C. & Su-Jae Lee
is a potential therapeutic target to Chaudhuri, N. Idiopathic Pulmonary Laboratory of Molecular Biochemistry,
restore progressive fibrotic disorders. Fibrosis (IPF): An Overview. J Clin Med Department of Life Science, Hanyang
7(2018). University, 222, Seoul 04763 Korea.
Phone: 82-2220-4554
E-mail: sj0420@hanyang.ac.kr