ArticleThe American journal of pathology2014
Protein tyrosine phosphatase α mediates profibrotic signaling in lung fibroblasts through TGF-β responsiveness.
Article in The American journal of pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 32 citations in OpenAlex.
- Mitogen-Activated Protein Kinase Phosphatase-5 is Required for TGF-β Signaling Through a JNK-Dependent Pathway.Molecular and cellular biology · 2025Article
- MAPK Phosphatase-5 is required for TGF-β signaling through a JNK-dependent pathway.bioRxiv : the preprint server for biology · 2024Article
- Article
- Clustering of phosphatase RPTPα promotes Src signaling and the arthritogenic action of synovial fibroblasts.Science signaling · 2023Article
- Targeting protein phosphatases in cancer immunotherapy and autoimmune disorders.Nature reviews. Drug discovery · 2023Review
- Saracatinib, a Selective Src Kinase Inhibitor, Blocks Fibrotic Responses in Preclinical Models of Pulmonary Fibrosis.American journal of respiratory and critical care medicine · 2022Article
- PTPα promotes fibroproliferative responses after acute lung injury.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- miR-486-5p Restrains Extracellular Matrix Production and Oxidative Damage in Human Trabecular Meshwork Cells by Targeting TGF-Journal of ophthalmology · 2022Article
- CD148 Deficiency in Fibroblasts Promotes the Development of Pulmonary Fibrosis.American journal of respiratory and critical care medicine · 2021Article
- Protein tyrosine phosphatase-α amplifies transforming growth factor-β-dependent profibrotic signaling in lung fibroblasts.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- RPTPα phosphatase activity is allosterically regulated by the membrane-distal catalytic domain.The Journal of biological chemistry · 2020Article
- Role of dual-specificity protein phosphatase DUSP10/MKP-5 in pulmonary fibrosis.American journal of physiology. Lung cellular and molecular physiology · 2019Article
- Loss of myeloid-specific protein phosphatase 2A enhances lung injury and fibrosis and results in IL-10-dependent sensitization of epithelial cell apoptosis.American journal of physiology. Lung cellular and molecular physiology · 2019Article
- The Importance of Tyrosine Phosphorylation Control of Cellular Signaling Pathways in Respiratory Disease: pY and pY Not.American journal of respiratory cell and molecular biology · 2018Review
- ILDgenDB: integrated genetic knowledge resource for interstitial lung diseases (ILDs).Database : the journal of biological databases and curation · 2018Article
- PTP4A1 promotes TGFβ signaling and fibrosis in systemic sclerosis.Nature communications · 2017Article
- Monocyte-derived alveolar macrophages drive lung fibrosis and persist in the lung over the life span.The Journal of experimental medicine · 2017Article
- Protein Tyrosine Phosphatases in Systemic Sclerosis: Potential Pathogenic Players and Therapeutic Targets.Current rheumatology reports · 2017Review
- Deficiency of α7 nicotinic acetylcholine receptor attenuates bleomycin-induced lung fibrosis in mice.Molecular medicine (Cambridge, Mass.) · 2017Article
- Taking It Off: New Insights into the Role of Tyrosine Phosphorylation-dependent Pathways in the Pathogenesis of Pulmonary Fibrosis.American journal of respiratory and critical care medicine · 2017Article
Corrections and comments
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Authors and funding
17 authors at 6 institutions in 3 countries.
Funding
Abstract
Fibrotic lung diseases represent a diverse group of progressive and often fatal disorders with limited treatment options. Although the pathogenesis of these conditions remains incompletely understood, receptor type protein tyrosine phosphatase α (PTP-α encoded by PTPRA) has emerged as a key regulator of fibroblast signaling. We previously reported that PTP-α regulates cellular responses to cytokines and growth factors through integrin-mediated signaling and that PTP-α promotes fibroblast expression of matrix metalloproteinase 3, a matrix-degrading proteinase linked to pulmonary fibrosis. Here, we sought to determine more directly the role of PTP-α in pulmonary fibrosis. Mice genetically deficient in PTP-α (Ptpra(-/-)) were protected from pulmonary fibrosis induced by intratracheal bleomycin, with minimal alterations in the early inflammatory response or production of TGF-β. Ptpra(-/-) mice were also protected from pulmonary fibrosis induced by adenoviral-mediated expression of active TGF-β1. In reciprocal bone marrow chimera experiments, the protective phenotype tracked with lung parenchymal cells but not bone marrow-derived cells. Because fibroblasts are key contributors to tissue fibrosis, we compared profibrotic responses in wild-type and Ptpra(-/-) mouse embryonic and lung fibroblasts. Ptpra(-/-) fibroblasts exhibited hyporesponsiveness to TGF-β, manifested by diminished expression of αSMA, EDA-fibronectin, collagen 1A, and CTGF. Ptpra(-/-) fibroblasts exhibited markedly attenuated TGF-β-induced Smad2/3 transcriptional activity. We conclude that PTP-α promotes profibrotic signaling pathways in fibroblasts through control of cellular responsiveness to TGF-β.
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Registered trials
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