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Tytuł pozycji:

Identification of Key Candidate Genes Involved in the Progression of Idiopathic Pulmonary Fibrosis.

Tytuł:
Identification of Key Candidate Genes Involved in the Progression of Idiopathic Pulmonary Fibrosis.
Autorzy:
Cui Y; Immunology and Reproduction Biology Laboratory & State Key Laboratory of Analytical Chemistry for Life Science, Medical School, Nanjing University, Hankou Road 22, Nanjing 210093, China.; Jiangsu Key Laboratory of Molecular Medicine, Nanjing University, Nanjing 210093, China.
Ji J; Immunology and Reproduction Biology Laboratory & State Key Laboratory of Analytical Chemistry for Life Science, Medical School, Nanjing University, Hankou Road 22, Nanjing 210093, China.; Jiangsu Key Laboratory of Molecular Medicine, Nanjing University, Nanjing 210093, China.
Hou J; Immunology and Reproduction Biology Laboratory & State Key Laboratory of Analytical Chemistry for Life Science, Medical School, Nanjing University, Hankou Road 22, Nanjing 210093, China.; Jiangsu Key Laboratory of Molecular Medicine, Nanjing University, Nanjing 210093, China.
Tan Y; Immunology and Reproduction Biology Laboratory & State Key Laboratory of Analytical Chemistry for Life Science, Medical School, Nanjing University, Hankou Road 22, Nanjing 210093, China.; Jiangsu Key Laboratory of Molecular Medicine, Nanjing University, Nanjing 210093, China.
Han X; Immunology and Reproduction Biology Laboratory & State Key Laboratory of Analytical Chemistry for Life Science, Medical School, Nanjing University, Hankou Road 22, Nanjing 210093, China.; Jiangsu Key Laboratory of Molecular Medicine, Nanjing University, Nanjing 210093, China.
Źródło:
Molecules (Basel, Switzerland) [Molecules] 2021 Feb 20; Vol. 26 (4). Date of Electronic Publication: 2021 Feb 20.
Typ publikacji:
Journal Article
Język:
English
Imprint Name(s):
Original Publication: Basel, Switzerland : MDPI, c1995-
MeSH Terms:
Idiopathic Pulmonary Fibrosis/*genetics
Annexin A3/genetics ; Collagen Type I/genetics ; Collagen Type I, alpha 1 Chain ; Databases, Genetic ; Gene Expression Profiling ; Gene Ontology ; Humans ; Insulin-Like Growth Factor I/genetics ; Integrin beta Chains/genetics ; Matrix Metalloproteinases/genetics ; Osteopontin/genetics ; Protein Interaction Maps ; Qa-SNARE Proteins/genetics ; Thrombospondins/genetics
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Grant Information:
81570059, 31370524 National Natural Science Foundation of China; BK20151398 the Natural Science Foundation of Jiangsu Province of China
Contributed Indexing:
Keywords: IGF-1; IPF; MMP; OPN; intergrin
Substance Nomenclature:
0 (ANXA3 protein, human)
0 (Collagen Type I)
0 (Collagen Type I, alpha 1 Chain)
0 (IGF1 protein, human)
0 (ITGB8 protein, human)
0 (Integrin beta Chains)
0 (Qa-SNARE Proteins)
0 (SPP1 protein, human)
0 (STX11 protein, human)
0 (Thrombospondins)
0 (thrombospondin 2)
106441-73-0 (Osteopontin)
67763-96-6 (Insulin-Like Growth Factor I)
EC 3.1.4.43 (Annexin A3)
EC 3.4.24.- (Matrix Metalloproteinases)
Entry Date(s):
Date Created: 20210306 Date Completed: 20210407 Latest Revision: 20211204
Update Code:
20240104
PubMed Central ID:
PMC7924352
DOI:
10.3390/molecules26041123
PMID:
33672678
Czasopismo naukowe
Idiopathic pulmonary fibrosis (IPF) is a lethal, agnogenic interstitial lung disease with limited therapeutic options. To investigate vital genes involved in the development of IPF, we integrated and compared four expression profiles (GSE110147, GSE53845, GSE24206, and GSE10667), including 87 IPF samples and 40 normal samples. By reanalyzing these datasets, we managed to identify 62 upregulated genes and 20 downregulated genes in IPF samples compared with normal samples. Differentially expressed genes (DEGs) were analyzed by gene ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis to illustrate relevant pathways of IPF, biological processes, molecular function, and cell components. The DEGs were then subjected to protein-protein interaction (PPI) for network analysis, serving to find 11 key candidate genes (ANXA3, STX11, THBS2, MMP1, MMP9, MMP7, MMP10, SPP1, COL1A1, ITGB8, IGF1). The result of RT-qPCR and immunohistochemical staining verified our finding as well. In summary, we identified 11 key candidate genes related to the process of IPF, which may contribute to novel treatments of IPF.
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