ArticleArthritis & rheumatology (Hoboken, N.J.)2015
Failed degradation of JunB contributes to overproduction of type I collagen and development of dermal fibrosis in patients with systemic sclerosis.
Article in Arthritis & rheumatology (Hoboken, N.J.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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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.
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Who cites it
31 citing papers in PubMed, 60 citations in OpenAlex.
- Preliminary analysis of chromatin accessibility in osteosarcoma tissues.Clinics (Sao Paulo, Brazil) · 2026Article
- Altered AP-1, RUNX, and EGR chromatin dynamics drive human fibrotic lung disease.Annals of the rheumatic diseases · 2026Article
- Chronic Rejection in Facial Vascularized Composite Allotransplantation (fVCA).Results and problems in cell differentiation · 2026Review
- Transcriptomic analysis reveals the impact of concurrent, resistance, and endurance training on skeletal muscle.PloS one · 2026Article
- Systemic sclerosis, main culprits and involved signaling pathways.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- Multi-omic analysis reveals retinoic acid molecular drivers for dermal fibrosis and regenerative repair in the skin.Cell stem cell · 2025Article
- Transcriptomic landscape around wound bed defines regenerative versus non-regenerative outcomes in mouse digit amputation.PLoS computational biology · 2025Article
- JunB condensation attenuates vascular endothelial damage under hyperglycemic condition.Journal of molecular cell biology · 2024Article
- Review
- Single-cell transcriptomics of hepatic stellate cells uncover crucial pathways and key regulators involved in non-alcoholic steatohepatitis.Endocrine connections · 2023Article
- Selection signature analyses and genome-wide association reveal genomic hotspot regions that reflect differences between breeds of horse with contrasting risk of degenerative suspensory ligament desmitis.G3 (Bethesda, Md.) · 2022Article
- Ticagrelor reduces doxorubicin-induced pyroptosis of rat cardiomyocytes by targeting GSK-3β/caspase-1.Frontiers in cardiovascular medicine · 2022Article
- Bushen Yijing Decoction (BSYJ) exerts an anti-systemic sclerosis effect via regulating MicroRNA-26a /FLI1 axis.Bioengineered · 2021Article
- Lutein attenuates angiotensin II- induced cardiac remodeling by inhibiting AP-1/IL-11 signaling.Redox biology · 2021Article
- Emerging Role of AP-1 Transcription Factor JunB in Angiogenesis and Vascular Development.International journal of molecular sciences · 2021Review
- CD47 prevents the elimination of diseased fibroblasts in scleroderma.JCI insight · 2020Article
- ETS2 promotes epithelial-to-mesenchymal transition in renal fibrosis by targeting JUNB transcription.Laboratory investigation; a journal of technical methods and pathology · 2020Article
- Glycogen synthase kinase-3β: a promising candidate in the fight against fibrosis.Theranostics · 2020Review
- [Focused ultrasound therapy for reducing recurrence of vulvar lichen simplex chronicus in rats: efficacy and mechanism].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2019Article
- Chronic rejection of human face allografts.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2019Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveThe excessive deposition of extracellular matrix, including type I collagen, is a key aspect in the pathogenesis of connective tissue diseases such as systemic sclerosis (SSc; scleroderma). To further our understanding of the mechanisms governing the dysregulation of type I collagen production in SSc, we investigated the role of the activator protein 1 (AP-1) family of transcription factors in regulating COL1A2 transcription.
methodsThe expression and nuclear localization of AP-1 family members (c-Jun, JunB, JunD, Fra-1, Fra-2, and c-Fos) were examined by immunohistochemistry and Western blotting in dermal biopsy specimens and explanted skin fibroblasts from patients with diffuse cutaneous SSc and healthy controls. Gene activation was determined by assessing the interaction of transcription factors with the COL1A2 enhancer using transient transfection of reporter gene constructs, electrophoretic mobility shift assays, chromatin immunoprecipitation analysis, and RNA interference involving knockdown of individual AP-1 family members. Inhibition of fibroblast mammalian target of rapamycin (mTOR), Akt, and glycogen synthase kinase 3β (GSK-3β) signaling pathways was achieved using small-molecule pharmacologic inhibitors.
resultsBinding of JunB to the COL1A2 enhancer was observed, with its coalescence directed by activation of gene transcription through the proximal promoter. Knockdown of JunB reduced enhancer activation and COL1A2 expression in response to transforming growth factor β. In SSc dermal fibroblasts, increased mTOR/Akt signaling was associated with inactivation of GSK-3β, leading to blockade of JunB degradation and, thus, constitutively high expression of JunB.
conclusionIn patients with SSc, the accumulation of JunB resulting from altered mTOR/Akt signaling and a failure of proteolytic degradation underpins the aberrant overexpression of type I collagen. These findings identify JunB as a potential target for antifibrotic therapy in SSc.
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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.