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miR-335-3p attenuates transforming growth factor beta 1-induced fibrosis by suppressing Thrombospondin 1open access
- Authors
- Han, Dong-Hee; Shin, Min Kyoung; Sung, Jung-Suk; Kim, Min
- Issue Date
- Oct-2024
- Publisher
- Public Library of Science
- Keywords
- Gelatinase A; Thrombospondin 1; Uvomorulin; 3' Untranslated Regions; Micrornas; Mirn335 Microrna, Human; Thrombospondin 1; Thrombospondin-1, Human; Transforming Growth Factor Beta1; Gelatinase A; Messenger Rna; Microrna; Microrna 335 3p; Mitogen Activated Protein Kinase 14; Thrombospondin 1; Transcription Factor Slug; Transcription Factor Snail; Transcriptome; Transforming Growth Factor Beta; Transforming Growth Factor Beta1; Unclassified Drug; Uvomorulin; Vimentin; Mirn335 Microrna, Human; Thrombospondin-1, Human; Airway Epithelium Cell; Angiogenesis; Article; Bioinformatics; Cell Invasion; Cell Migration; Cell Proliferation; Cell Survival; Cell Viability; Controlled Study; Cytotoxicity; Down Regulation; Epithelial Mesenchymal Transition; Extracellular Matrix; Fluorescence Imaging; Gene Expression; Gene Ontology; Gene Silencing; Genetic Transfection; Human; Human Cell; Immunoblotting; Immunofluorescence Assay; Intracellular Signaling; Luciferase Assay; Lung Fibrosis; Microarray Analysis; Mtt Assay; Protein Expression; Protein Protein Interaction; Real Time Polymerase Chain Reaction; Reverse Transcription Polymerase Chain Reaction; Rna Isolation; Rna Sequence; Upregulation; Western Blotting; Wound Healing; 3' Untranslated Region; Animal; Cell Line; Drug Effect; Epithelium Cell; Genetics; Male; Metabolism; Mouse; Pathology; Signal Transduction; 3' Untranslated Regions; Animals; Cell Line; Epithelial Cells; Epithelial-mesenchymal Transition; Humans; Male; Mice; Micrornas; Pulmonary Fibrosis; Signal Transduction; Thrombospondin 1; Transforming Growth Factor Beta1
- Citation
- PLoS ONE, v.19, no.10, pp 1 - 16
- Pages
- 16
- Indexed
- SCIE
SCOPUS
- Journal Title
- PLoS ONE
- Volume
- 19
- Number
- 10
- Start Page
- 1
- End Page
- 16
- ISSN
- 1932-6203
1932-6203
- Abstract
- Pulmonary fibrosis is characterized by excessive extracellular matrix (ECM) accumulation caused by detrimental stimuli. The progressive impairment in lung functions is chronic and highly fatal, presenting itself as a global health challenge. Because of the lack of efficacious treatments, the underlying mechanism should be investigated. The progression of fibrosis involves transforming growth factor-beta 1 (TGF-beta 1), which accelerates ECM production via epithelial-mesenchymal transition and cell invasion. As microRNAs (miRNAs) serve as regulators of disease development and progression, this study aimed to investigate the interaction of miRNAs and target genes that could contribute to pulmonary fibrosis when exposed to TGF-beta 1. Differentially expressed mRNA and miRNA were identified in respiratory epithelial cells via transcriptome analysis by using the constructed TGF-beta 1-induced fibrosis model. Our results revealed a significant increase in the expression of thrombospondin 1 (THBS1), which participates in TGF-beta 1 activation, where THBS1 was identified as a core gene in protein interactions analyzed through bioinformatics. The expression of miR-335-3p, which targets 3 '-UTR of THBS1, substantially decreased upon TGF-beta 1 treatment. The TGF-beta 1 downstream signal was suppressed by inhibiting the interaction between TGF-beta 1 and THBS1, consequently alleviating fibrosis. When the miR-335-3p mimic was transfected in TGF-beta 1-treated respiratory epithelial cells, THBS1 and fibrosis markers were downregulated, while the introduction of miR-335-3p inhibitor exhibited a reverse phenomenon. Our findings demonstrated that TGF-beta 1 exposure to respiratory epithelial cells led to a decrease in miR-335-3p expression, resulting in the upregulation of THBS1 and ultimately exacerbating fibrosis. This study provides insights into TGF-beta 1-induced pulmonary fibrosis, suggesting new therapeutic targets and mechanisms.
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Related Researcher
- Sung, Jung Suk
- College of Life Science and Biotechnology (Department of Life Science)