ArticlePloS one2015
Vimentin Phosphorylation Underlies Myofibroblast Sensitivity to Withaferin A In Vitro and during Corneal Fibrosis.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
21 citing papers in PubMed, 34 citations in OpenAlex.
- Differential Cytoskeletal Control of Cell-Collagen Mechanics in High- and Low-Flow Glaucomatous Trabecular Meshwork Cells.ACS applied materials & interfaces · 2026Article
- Silencing Ubiquitin-Specific Peptidase 10 Alleviates Persistent Corneal Epithelial Defect in Mice.The American journal of pathology · 2026Article
- Discovery of Trametinib as an orchestrator for cytoskeletal vimentin remodeling.Journal of molecular cell biology · 2024Article
- The Role of Vimentin in Human Corneal Fibroblast Spreading and Myofibroblast Transformation.Cells · 2024Article
- Vimentin-mediated buffering of internal integrin β1 pool increases survival of cells from anoikis.BMC biology · 2024Article
- Interferon-induced MXB protein restricts vimentin-dependent viral infection.Acta pharmaceutica Sinica. B · 2024Article
- Roles of vimentin in health and disease.Genes & development · 2022Review
- Cytoskeleton Reorganization in EndMT-The Role in Cancer and Fibrotic Diseases.International journal of molecular sciences · 2021Review
- Article
- Keratocyte mechanobiology.Experimental eye research · 2020Review
- Article
- Desmin deficiency is not sufficient to prevent corneal fibrosis.Experimental eye research · 2019Article
- The Physicochemical Properties of Decellularized Extracellular Matrix-Coated 3D Printed Poly(ε-caprolactone) Nerve Conduits for Promoting Schwann Cells Proliferation and Differentiation.Materials (Basel, Switzerland) · 2018Article
- Sustained activation of ERK1/2 MAPK in Schwann cells causes corneal neurofibroma.Journal of neuroscience research · 2017Article
- USP14 de-ubiquitinates vimentin and miR-320a modulates USP14 and vimentin to contribute to malignancy in gastric cancer cells.Oncotarget · 2017Article
- Expression of peptidylarginine deiminase 4 in an alkali injury model of retinal gliosis.Biochemical and biophysical research communications · 2017Article
- Effect of Different Antibiotic Chemotherapies onFrontiers in microbiology · 2017Article
- Galectin-3 Inhibition by a Small-Molecule Inhibitor Reduces Both Pathological Corneal Neovascularization and Fibrosis.Investigative ophthalmology & visual science · 2017Article
- Pharmacologic inhibition of reactive gliosis blocks TNF-α-mediated neuronal apoptosis.Cell death & disease · 2016Article
- Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Vimentin is a newly recognized target for corneal fibrosis. Using primary rabbit corneal fibroblasts and myofibroblasts we show that myofibroblasts, unlike fibroblasts, display impaired cell spreading and cell polarization, which is associated with increased levels of soluble serine-38 phosphorylated vimentin (pSer38Vim). This pSer38Vim isoform is inefficiently incorporated into growing vimentin intermediate filaments (IFs) of myofibroblasts during cell spreading, and as a result, myofibroblasts maintain higher soluble pSer38Vim levels compared to fibroblasts. Moreover, the soluble vimentin-targeting small molecule and fibrotic inhibitor withaferin A (WFA) causes a potent blockade of cell spreading selectively in myofibroblasts by targeting soluble pSer38Vim for hyperphosphorylation. WFA treatment does not induce vimentin hyperphosphorylation in fibroblasts. This hyperphosphorylated pSer38Vim species in WFA-treated myofibroblasts becomes complexed with adaptor protein filamin A (FlnA), and these complexes appear as short squiggles when displaced from focal adhesions. The extracellular-signal regulated kinase (ERK) is also phosphorylated (pERK) in response to WFA, but surprisingly, pERK does not enter the nucleus but remains bound to pSer38Vim in cytoplasmic complexes. Using a model of corneal alkali injury, we show that fibrotic corneas of wild type mice possess high levels of pERK, whereas injured corneas of vimentin-deficient (Vim KO) mice that heal with reduced fibrosis have highly reduced pERK expression. Finally, WFA treatment causes a decrease in pERK and pSer38Vim expression in healing corneas of wild type mice. Taken together, these findings identify a hereto-unappreciated role for pSer38Vim as an important determinant of myofibroblast sensitivity to WFA.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.