ArticlePloS one2013
Downregulation of OPA3 is responsible for transforming growth factor-β-induced mitochondrial elongation and F-actin rearrangement in retinal pigment epithelial ARPE-19 cells.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Intrinsic TGF-β signaling attenuates proximal tubule mitochondrial injury and inflammation in chronic kidney disease.Nature communications · 2023Article
- Loss of KMT5C Promotes EGFR Inhibitor Resistance in NSCLC via LINC01510-Mediated Upregulation of MET.Cancer research · 2022Article
- Butyrate Prevents TGF-β1-Induced Alveolar Myofibroblast Differentiation and Modulates Energy Metabolism.Metabolites · 2021Article
- Molecular Mechanisms behind Inherited Neurodegeneration of the Optic Nerve.Biomolecules · 2021Review
- Oncogenic K-ras Induces Mitochondrial OPA3 Expression to Promote Energy Metabolism in Pancreatic Cancer Cells.Cancers · 2019Article
- Autosomal dominant optic atrophy and cataract "plus" phenotype including axonal neuropathy.Neurology. Genetics · 2019Article
- TGF-β2 initiates autophagy via Smad and non-Smad pathway to promote glioma cells' invasion.Journal of experimental & clinical cancer research : CR · 2017Article
- The mitochondrial fusion-related proteins Mfn2 and OPA1 are transcriptionally induced during differentiation of bone marrow progenitors to immature dendritic cells.Molecules and cells · 2015Article
- Cancer cells exploit adaptive mitochondrial dynamics to increase tumor cell invasion.Cell cycle (Georgetown, Tex.) · 2015Review
- Mitochondrial dynamic changes in health and genetic diseases.Molecular biology reports · 2014Review
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Authors and funding
5 authors at 1 institution in 1 country.
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Abstract
Transforming growth factor-β signaling is known to be a key signaling pathway in the induction of epithelial-mesenchymal transition. However, the mechanism of TGF-β signaling in the modulation of EMT remains unclear. In this study, we found that TGF-β treatment resulted in elongation of mitochondria accompanied by induction of N-cadherin, vimentin, and F-actin in retinal pigment epithelial cells. Moreover, OPA3, which plays a crucial role in mitochondrial dynamics, was downregulated following TGF-β treatment. Suppression of TGF-β signaling using Smad2 siRNA prevented loss of OPA3 induced by TGF-β. Knockdown of OPA3 by siRNA and inducible shRNA significantly increased stress fiber levels, cell length, cell migration and mitochondrial elongation. In contrast, forced expression of OPA3 in ARPE-19 cells inhibited F-actin rearrangement and induced mitochondrial fragmentation. We also showed that Drp1 depletion increased cell length and induced rearrangement of F-actin. Depletion of Mfn1 blocked the increase in cell length during TGF-β-mediated EMT. These results collectively substantiate the involvement of mitochondrial dynamics in TGF-β-induced EMT.
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