ArticleJournal of cellular and molecular medicine2013
Epigenetic repression of bone morphogenetic protein receptor II expression in scleroderma.
Article in Journal of cellular and molecular medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
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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
35 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Unfolding the pathogenesis of scleroderma through genomics and epigenomics.Journal of autoimmunity · 2017Pooled it
- Trial
- TGF-β-induced epigenetic deregulation of SOCS3 facilitates STAT3 signaling to promote fibrosis.The Journal of clinical investigation · 2020Trial
- Review
- DNA methylation in human diseases.Heliyon · 2024Review
- Recent Insights into the Role of DNA Methylation and Histone Modifications in Systemic Sclerosis: A Scoping Review.Diagnostics (Basel, Switzerland) · 2024Article
- The critical importance of epigenetics in autoimmune-related skin diseases.Frontiers of medicine · 2023Review
- The Evolving Management and Treatment Options for Patients with Pulmonary Hypertension: Current Evidence and Challenges.Vascular health and risk management · 2023Review
- Genome-wide DNA methylation pattern in systemic sclerosis microvascular endothelial cells: Identification of epigenetically affected key genes and pathways.Journal of scleroderma and related disorders · 2022Article
- Epigenetic Modifications in the Pathogenesis of Systemic Sclerosis.International journal of general medicine · 2022Review
- Advances in epigenetics in systemic sclerosis: molecular mechanisms and therapeutic potential.Nature reviews. Rheumatology · 2021Review
- Non-Coding RNA in Systemic Sclerosis: A Valuable Tool for Translational and Personalized Medicine.Genes · 2021Review
- Epigenetic down-regulation of microRNA-126 in scleroderma endothelial cells is associated with impaired responses to VEGF and defective angiogenesis.Journal of cellular and molecular medicine · 2021Article
- Epigenetic Targets for Oligonucleotide Therapies of Pulmonary Arterial Hypertension.International journal of molecular sciences · 2020Review
- Epigenetics and systemic sclerosis: An answer to disease onset and evolution?European journal of rheumatology · 2020Review
- The contribution of epigenetics to the pathogenesis and gender dimorphism of systemic sclerosis: a comprehensive overview.Therapeutic advances in musculoskeletal disease · 2020Review
- Epigenetic Control of Scleroderma: Current Knowledge and Future Perspectives.Current rheumatology reports · 2019Review
- Epigenetics of scleroderma: Integrating genetic, ethnic, age, and environmental effects.Journal of scleroderma and related disorders · 2019Review
- Identification of Cysteine-Rich Angiogenic Inducer 61 as a Potential Antifibrotic and Proangiogenic Mediator in Scleroderma.Arthritis & rheumatology (Hoboken, N.J.) · 2019Article
- Unmet Needs in Systemic Sclerosis Understanding and Treatment: the Knowledge Gaps from a Scientist's, Clinician's, and Patient's Perspective.Clinical reviews in allergy & immunology · 2018Review
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Germline mutations in the bone morphogenetic protein type II receptor (BMPRII) gene play an essential role in the pathogenesis of familial pulmonary arterial hypertension (FPAH). In view of the histological similarities between scleroderma (SSc) and FPAH arterial lesion, we examined the expression levels of BMPRII in SSc microvascular endothelial cells (MVEC). Oxidative stress and serum starvation were used to examine apoptotic responses of MVECs. BMPRII expression levels were determined by RT-PCR and by Western blot. Epigenetic regulation of BMPRII expression was examined by the addition of epigenetic inhibitors to MVECs cultures, by methylation-specific PCR, and by sequence analysis of DNA methylation pattern of the BMPRII promotor region. SSc-MVECs were more sensitive to apoptotic signals than were normal-MVECs. A significant decrease in BMPRII expression levels in SSc-MVECs was noted, whereas no significant differences in the expression levels of BMPRIA and BMPRIB were observed. Similar reduction in expression levels was noted in SSc skin biopsies. The expression level of BMPRII in SSc-MVECs was normalized by the addition of 2-deoxy-5-azacytidine and trichostatin A to cell cultures. Extensive CpG sites methylation in the BMPRII promoter region was noted in SSc-MVECs with no detectable site methylation in control-MVECs. SSc-MVECs are more sensitive to apoptotic triggers than are control-MVECs. The enhanced apoptosis may be related to epigenetic repression of BMPRII expression as apoptosis of control-MVECs can be augmented by knocking down BMPRII expression. The role of BMPRII underexpression in the pathogenesis of SSc vasculopathy is suggested and should be investigated further.
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