Journal
JOURNAL OF THORACIC DISEASE
Volume 9, Issue 3, Pages 519-528Publisher
AME PUBL CO
DOI: 10.21037/jtd.2017.02.50
Keywords
Idiopathic nonspecific interstitial pneumonia (INSIP); idiopathic pulmonary fibrosis (IPF); transforming growth factor-beta-1 (TGF-beta 1); fibroblast growth factor 10 (FGF10); platelet derived growth factor (PDGF)
Categories
Funding
- Science and Technology Commission Foundation of Key Medical Research Foundation of Shanghai, China [034119868, 09411951600]
- Key Medical Research Foundation of the Health Bureau of Shanghai, China [20134034]
- National Nature Science Foundation of China [81570053]
Ask authors/readers for more resources
Background: Idiopathic nonspecific interstitial pneumonia (INSIP) presents with varying degrees of interstitial inflammation and fibrosis exhibiting a uniform appearance. Lack of knowledge on the underlying mechanisms of INSIP has contributed to few effective treatment strategies. Our study is designed to explore aberrantly expressed cytokines involvement in INSIP development. Methods: Oligo GEArray was employed to detect the expression of cytokines in INSIP patients, and idiopathic pulmonary fibrosis (IPF) was setup as isotype control. Real-time PCR and immunohistochemistry analysis were used to further confirm the expression of abnormally expressed cytokines. The correlationship between cytokines expression and overall survival rate of patients with IPF and INSIP were analyzed. Results: From microarray detection, transforming growth factor-beta-1 (TGF-beta 1), fibroblast growth factor 10 (FGF10), and platelet derived growth factor (PDGF) were predominantly up-regulated in patients with INSIP. Real-time PCR and immunohistochemistry also showed these cytokines was abnormally expressed in INSIP. In addition to, the clinical relevance analysis demonstrated relatively lower expression of PDGF patients had longer overall survival rate than those with higher expression of PDGF. Conclusions: Our study suggests that TGF-beta 1, FGF10, and PDGF are required for the pathogenesis of INSIP, and may therefore be ideal targets in INSIP treatment. Moreover, INSIP patients with lower expression of PDGF had better survival rate.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available