Journal
INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE
Volume 32, Issue 2, Pages 355-364Publisher
SPANDIDOS PUBL LTD
DOI: 10.3892/ijmm.2013.1404
Keywords
lung fibrosis; long non-coding RNA; microassay; AJ005396; S69206
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Funding
- National Natural Science Foundation of China [81273957]
- Important Project of Science and Technology of Shandong Province [2010GWZ20254, 2011GHY11501]
- Natural Science Foundation of Shandong Province [ZR2009EM006, ZR2012HQ042]
- Project of Science and Technology of the Education Department of Shandong Province [J11FL87]
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Recent studies suggest that long non-coding RNAs (lncRNAs) are more involved in human diseases than previously realized. A growing body of evidence links lncRNA mutation and dysregulation to diverse human diseases. However, the association of lncRNAs with the pathogenesis of lung fibrosis remains poorly understood. In this study, we detected changes in hydroxyproline and collagen levels, as well as the ultrastructure of lung tissue to develop a rat model of lung fibrosis. The differentially expressed lncRNAs and mRNA profiles between fibrotic lung and normal lung tissue were analyzed using micro-arrays. Gene Ontology analysis and pathway analysis were performed for further research. Two differentially expressed lncRNAs, namely, AJ005396 and S69206, were detected by in situ hybridization to validate the microarray data. The results revealed that the number of collagen fibers in the interstitial lung tissue significantly increased in the model group compared with the normal group. In total, 210 and 358 lncRNAs were upregulated and downregulated, respectively, along with 415 upregulated and 530 downregulated mRNAs in the rats with lung fibrosis. AJ005396 and S69206 were upregulated in the fibrotic lung tissue, consistent with the microarray data, and were located in the cytoplasm of the interstitial lung cells. In conclusion, the expression profile of the lncRNAs was significantly altered in the fibrotic lung tissue and these transcripts are potential molecular targets for inhibiting the development of lung fibrosis.
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