ArticleArthritis research & therapy2018
Blocking CD248 molecules in perivascular stromal cells of patients with systemic sclerosis strongly inhibits their differentiation toward myofibroblasts and proliferation: a new potential target for antifibrotic therapy.
Article in Arthritis research & therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 37 citations in OpenAlex.
- Cysteine addiction in drug resistant glioblastoma and therapeutic targeting with designer selenium compounds.Neuro-oncology · 2026Article
- Distinct landscapes of fibroblast subtypes in arteries of patients with giant cell arteritis.Rheumatology (Oxford, England) · 2025Article
- Pan-cancer analysis identified CD248 as a potential target for multiple tumor types.Frontiers in pharmacology · 2025Article
- The Hidden Hand in White Matter: Pericytes and the Puzzle of Demyelination.ACS pharmacology & translational science · 2024Review
- CD248-expressing cancer-associated fibroblasts induce non-small cell lung cancer metastasis via Hippo pathway-mediated extracellular matrix stiffness.Journal of cellular and molecular medicine · 2024Article
- Adipose-Derived Stromal Cell-Based Therapies for Radiation-Induced Fibrosis.Advances in wound care · 2024Review
- [Expression of endosialin in human hypertrophic scars and its regulation on fibroblast phenotype].Zhonghua shao shang yu chuang mian xiu fu za zhi · 2023Article
- Mesenchymal stem cell-based therapy for autoimmune-related fibrotic skin diseases-systemic sclerosis and sclerodermatous graft-versus-host disease.Stem cell research & therapy · 2023Review
- Novel piperazine-based ionizable lipid nanoparticles allow the repeated dose of mRNA to fibrotic lungs with improved potency and safety.Bioengineering & translational medicine · 2023Article
- Tofacitinib May Inhibit Myofibroblast Differentiation from Rheumatoid-Fibroblast-like Synoviocytes Induced by TGF-β and IL-6.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Cd248a and Cd248b in zebrafish participate in innate immune responses.Frontiers in immunology · 2022Article
- Endothelial-to-mesenchymal transition in systemic sclerosis.Clinical and experimental immunology · 2021Review
- New Insights into Profibrotic Myofibroblast Formation in Systemic Sclerosis: When the Vascular Wall Becomes the Enemy.Life (Basel, Switzerland) · 2021Review
- Metabolic consequences for mice lacking Endosialin: LC-MS/MS-based metabolic phenotyping of serum from C56Bl/6J Control and CD248 knock-out mice.Metabolomics : Official journal of the Metabolomic Society · 2021Article
- CD248 as a novel therapeutic target in pulmonary arterial hypertension.Clinical and translational medicine · 2020Article
- Pro-inflammatory properties of H-ferritin on human macrophages, ex vivo and in vitro observations.Scientific reports · 2020Article
- Interleukin-32 in systemic sclerosis, a potential new biomarker for pulmonary arterial hypertension.Arthritis research & therapy · 2020Article
- CD248 and integrin alpha-8 are candidate markers for differentiating lung fibroblast subtypes.BMC pulmonary medicine · 2020Article
- Mesenchymal Stromal Cells Anno 2019: Dawn of the Therapeutic Era? Concise Review.Stem cells translational medicine · 2019Review
- C-type lectin domain group 14 proteins in vascular biology, cancer and inflammation.The FEBS journal · 2019Review
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundFibrosis may be considered the hallmark of systemic sclerosis (SSc), the end stage triggered by different pathological events. Transforming growth factor-β (TGF-β) and platelet-derived growth factor BB (PDGF-BB) are profibrotic molecules modulating myofibroblast differentiation and proliferation, respectively. There is evidence linking CD248 with these two molecules, both highly expressed in patients with SSc, and suggesting that CD248 may be a therapeutic target for several diseases. The aim of this work was to evaluate the expression of CD248 in SSc skin and its ability to modulate SSc fibrotic process.
methodsAfter ethical approval was obtained, skin biopsies were collected from 20 patients with SSc and 10 healthy control subjects (HC). CD248 expression was investigated in the skin, as well as in bone marrow mesenchymal stem cells (MSCs) treated with TGF-β or PDGF-BB, by immunofluorescence, qRT-PCR, and Western blotting. Finally, in SSc-MSCs, the CD248 gene was silenced by siRNA.
resultsIncreased expression of CD248 was found in endothelial cells and perivascular stromal cells of SSc skin. In SSc-MSCs, the levels of CD248 and α-smooth muscle actin expression were significantly higher than in HC-MSCs. In both SSc- and HC-MSCs, PDGF-BB induced increased expression of Ki-67 when compared with untreated cells but was unable to modulate CD248 levels. After CD248 silencing, both TGF-β and PDGF-BB signaling were inhibited in SSc-MSCs.
conclusionsCD248 overexpression may play an important role in the fibrotic process by modulating the molecular target, leading to perivascular cells differentiation toward myofibroblasts and interfering with its expression, and thus might open a new therapeutic strategy to inhibit myofibroblast generation during SSc.
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