ArticleJournal of immunology (Baltimore, Md. : 1950)2018
RGC32 Promotes Bleomycin-Induced Systemic Sclerosis in a Murine Disease Model by Modulating Classically Activated Macrophage Function.
Article in Journal of immunology (Baltimore, Md. : 1950), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 23 citations in OpenAlex.
- Monocytes strongly induce (myo)fibroblast contraction in a 3D skin model to understand inflammation-fibrosis crosstalk.Scientific reports · 2026Article
- Behavior of Complement System Effectors in Chronic and Acute Coronary Artery Disease.Journal of clinical medicine · 2025Article
- The role of immune cells in the pathogenesis of connective tissue diseases-associated pulmonary arterial hypertension.Frontiers in immunology · 2024Review
- The Role of Macrophages in Connective Tissue Disease-Associated Interstitial Lung Disease: Focusing on Molecular Mechanisms and Potential Treatment Strategies.International journal of molecular sciences · 2023Review
- Macrophage: Key player in the pathogenesis of autoimmune diseases.Frontiers in immunology · 2023Review
- IL-33/Regulatory T-Cell Axis Suppresses Skin Fibrosis.The Journal of investigative dermatology · 2022Article
- Regulator of Cell Cycle Protein (RGCC/RGC-32) Protects against Pulmonary Fibrosis.American journal of respiratory cell and molecular biology · 2022Article
- Pumping the Brakes on Pulmonary Fibrosis: A New Role for Regulator of Cell Cycle.American journal of respiratory cell and molecular biology · 2022Article
- ADAR1 promotes systemic sclerosisFrontiers in immunology · 2022Article
- Role of RGC-32 in multiple sclerosis and neuroinflammation - few answers and many questions.Frontiers in immunology · 2022Review
- RGCC balances self-renewal and neuronal differentiation of neural stem cells in the developing mammalian neocortex.EMBO reports · 2021Article
- Pulmonary involvement in systemic sclerosis: exploring cellular, genetic and epigenetic mechanisms.Rheumatology international · 2020Review
- LncRNA GAS5 attenuates fibroblast activation through inhibiting Smad3 signaling.American journal of physiology. Cell physiology · 2020Article
- RGC-32 and diseases: the first 20 years.Immunologic research · 2019Review
- Autoimmunity in 2018.Clinical reviews in allergy & immunology · 2019Article
- Response by Cui et al to Letter Regarding Article, "RGC-32 (Response Gene to Complement 32) Deficiency Protects Endothelial Cells From Inflammation and Attenuates Atherosclerosis".Arteriosclerosis, thrombosis, and vascular biology · 2018Article
- Response Gene to Complement 32 in Vascular Diseases.Frontiers in cardiovascular medicine · 2018Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Systemic sclerosis (SSc) is a multisystem autoimmune disorder that is characterized by inflammation and fibrosis in the skin and internal organs. Previous studies indicate that inflammatory cells and cytokines play essential roles in the pathogenesis of SSc; however, the mechanisms that underlie the inflammation-driven development of SSc are not fully understood. In this study, we show that response gene to complement 32 (RGC32) is abundantly expressed in mouse macrophages in the early stage of bleomycin-induced SSc. Importantly, RGC32 is required to induce the inflammatory response during the onset of SSc, because RGC32 deficiency in mice significantly ameliorates skin and lung sclerosis and inhibits the expression of inflammatory mediators inducible NO synthase (iNOS) and IL-1β in macrophages. RGC32 appears to be a novel regulator for the differentiation of classically activated macrophages (M1 macrophages). IFN-γ and LPS stimulation induces RGC32 expression in primary peritoneal macrophages and bone marrow-derived macrophages. RGC32 deficiency impairs the polarization of M1 macrophages and attenuates iNOS and IL-1β production. Mechanistically, RGC32 interacts with NF-κB proteins and promotes iNOS and IL-1β expression by binding to their promoters. Collectively, our data reveal that RGC32 promotes the onset of SSc by regulating the inflammatory response of M1 macrophages, and it may serve as a promising therapeutic target for treating 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.