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TGF-β regulates TGFBIp expression in corneal fibroblasts via miR-21, miR-181a, and Smad signaling

Authors
 Seung-il Choi  ;  Jun-Yup Jin  ;  Yong-Sun Maeng  ;  Tae-im Kim  ;  Eung Kweon Kim 
Citation
 Biochemical and Biophysical Research Communications, Vol.472(1) : 150-155, 2016 
Journal Title
 Biochemical and Biophysical Research Communications 
ISSN
 0006-291X 
Issue Date
2016
MeSH
Cells, Cultured ; Cornea/cytology ; Cornea/metabolism* ; Corneal Dystrophies, Hereditary/genetics ; Corneal Dystrophies, Hereditary/metabolism ; Corneal Dystrophies, Hereditary/pathology ; Extracellular Matrix Proteins/genetics* ; Extracellular Matrix Proteins/metabolism* ; Fibroblasts/cytology ; Fibroblasts/metabolism ; Gene Expression Regulation ; Homozygote ; Humans ; MicroRNAs/genetics* ; MicroRNAs/metabolism* ; Models, Biological ; Mutant Proteins/genetics ; Mutant Proteins/metabolism ; Point Mutation ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Signal Transduction ; Smad Proteins/metabolism* ; Transforming Growth Factor beta/genetics* ; Transforming Growth Factor beta/metabolism* ; Transforming Growth Factor beta1/metabolism*
Keywords
Corneal fibroblasts ; Granular corneal dystrophy type 2 ; TGF-β ; TGFBI ; TGFBIp ; microRNA
Abstract
Transforming growth factor-β (TGF-β)-induced gene (TGFBI) protein (TGFBIp) is associated with granular corneal dystrophy type 2 (GCD2). TGFBIp levels can affect GCD2 phenotypes, but the underlying molecular mechanisms have not been fully elucidated. We investigated the involvement of microRNA (miRNA) and TGF-β in the regulation of TGFBIp expression in corneal fibroblasts. Ectopic expression of miR-9, miR-21, and miR-181a significantly decreased TGFBIp levels. Conversely, expression of miR-21 and miR-181a was induced by TGF-β1. Expression of miR-21 was 10-fold higher than that of miR-9 and miR-181a in corneal fibroblasts. Additionally, TGF-β1 expression was significantly higher than that of TGF-β2 and TGF-β3 in corneal fibroblasts, whereas expression of all three TGF-β forms was not significantly different between wild-type (WT) and GCD2 homozygotes (HO) corneal fibroblasts. Taken together, these data indicate that TGFBIp expression is positively regulated by TGF-β, whereas TGF-β-induced miR-21 and miR-181a negatively regulate TGFBIp expression. In conclusion, TGFBIp levels in corneal fibroblasts are controlled via the coordinated activity of miR-21 and miR-181a and by Smad signaling. Pharmacologic modulation of these miRNAs and TGF-β signaling could have therapeutic potential for TGFBI-associated corneal dystrophy, including GCD2.
Full Text
http://www.sciencedirect.com/science/article/pii/S0006291X16302753
DOI
10.1016/j.bbrc.2016.02.086
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Ophthalmology (안과학교실) > 1. Journal Papers
5. Research Institutes (연구소) > Corneal Dystrophy Research Institute (각막이상증연구소) > 1. Journal Papers
Yonsei Authors
김응권(Kim, Eung Kweon) ORCID logo https://orcid.org/0000-0002-1453-8042
김태임(Kim, Tae Im) ORCID logo https://orcid.org/0000-0001-6414-3842
맹용선(Maeng, Yong Sun) ORCID logo https://orcid.org/0000-0003-1694-8405
최승일(Choi, Seung Il) ORCID logo https://orcid.org/0000-0001-7168-8795
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URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/146486
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