ArticleFibrogenesis & tissue repair2015
Enhanced chemokine-receptor expression, function, and signaling in healthy African American and scleroderma-patient monocytes are regulated by caveolin-1.
Article in Fibrogenesis & tissue repair, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 41 citations in OpenAlex.
- Site-Specific Phosphoproteomic Profiling of CAV1 Reveals Co-Regulatory Kinase Networks in Cancer Signaling.International journal of molecular sciences · 2026Article
- Cav-1 deficiency induces cardiac dysfunction via the AdipoR1-AMPK-mTOR autophagy pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Revolutionizing Autoimmune Research: The Role of Caveolin-1.Immunity, inflammation and disease · 2025Review
- CD45+/ Col I+ Fibrocytes: Major source of collagen in the fibrotic lung, but not in passaged fibroblast cultures.Matrix biology : journal of the International Society for Matrix Biology · 2025Article
- Review
- The Role of CCL24 in Systemic Sclerosis.Rambam Maimonides medical journal · 2023Review
- Therapeutic Approaches to Systemic Sclerosis: Recent Approvals and Future Candidate Therapies.Clinical reviews in allergy & immunology · 2023Review
- Immunophenotyping of Monocyte Migration Markers and Therapeutic Effects of Selenium on IL-6 and IL-1β Cytokine Axes of Blood Mononuclear Cells in Preoperative and Postoperative Coronary Artery Disease Patients.International journal of molecular sciences · 2023Article
- Distinct genome-wide DNA methylation and gene expression signatures in classical monocytes from African American patients with systemic sclerosis.Clinical epigenetics · 2023Article
- Pyroptosis executor gasdermin D plays a key role in scleroderma and bleomycin-induced skin fibrosis.Cell death discovery · 2022Article
- Multiple subregions within the caveolin-1 scaffolding domain inhibit fibrosis, microvascular leakage, and monocyte migration.PloS one · 2022Article
- Intimate intertwining of the pathogenesis of hypoxia and systemic sclerosis: A transcriptome integration analysis.Frontiers in immunology · 2022Article
- Involvement of caveolin-1 in skin diseases.Frontiers in immunology · 2022Review
- The Caveolin-1 Scaffolding Domain Peptide Reverses Aging-Associated Deleterious Changes in Multiple Organs.The Journal of pharmacology and experimental therapeutics · 2021Article
- Butyrate Improves Skin/Lung Fibrosis and Intestinal Dysbiosis in Bleomycin-Induced Mouse Models.International journal of molecular sciences · 2021Article
- The importance of caveolins and caveolae to dermatology: Lessons from the caves and beyond.Experimental dermatology · 2020Review
- Fli1 Downregulation in Scleroderma Myeloid Cells Has Profibrotic and Proinflammatory Effects.Frontiers in immunology · 2020Article
- Trained immunity modulates inflammation-induced fibrosis.Nature communications · 2019Article
- Whole-genome bisulfite sequencing in systemic sclerosis provides novel targets to understand disease pathogenesis.BMC medical genomics · 2019Article
- Epigenetics of scleroderma: Integrating genetic, ethnic, age, and environmental effects.Journal of scleroderma and related disorders · 2019Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
backgroundA major health disparity suffered by African Americans (AA) is a predisposition toward fibrotic diseases of the skin, lung, and other organs. We previously showed that healthy AA and scleroderma (systemic sclerosis (SSc)) patient monocytes share biochemical and functional differences from control Caucasian (C) monocytes that may predispose AA to SSc. The central difference is a decrease in caveolin-1. Low caveolin-1 levels promote monocyte migration, their differentiation into fibrocytes, and fibrocyte recruitment into fibrotic tissues. Here we have greatly expanded our studies on the mechanism of action in fibrosis of caveolin-1 in AA and SSc monocytes.
resultsExpression of chemokine receptors (CCR1, CCR2, CCR3) is enhanced in healthy AA monocytes compared to healthy C monocytes and further increased in SSc monocytes. A parallel increase in function occurs assessed by migration toward chemokines MCP-1 and MCP-3. Chemokine-receptor expression and function are inhibited by the caveolin-1 scaffolding domain peptide (CSD) via its action as a surrogate for caveolin-1. Cells bearing chemokine receptors accumulate to high levels in fibrotic lung and skin tissue from SSc patients and from mice treated with bleomycin. This accumulation is almost completely blocked in mice treated with CSD. In signaling studies, Src activation is enhanced in AA monocytes compared to C monocytes and further increased in SSc monocytes. Lyn is also highly activated in SSc monocytes. Src and Lyn activation are inhibited by CSD. Src and Lyn's roles in monocyte migration were demonstrated using specific inhibitors.
conclusionsTo the best of our knowledge, this is the first report that the expression and function of CCR1, CCR2, and CCR3 are upregulated in monocytes from healthy AA and from SSc patients via molecular mechanisms involving caveolin-1, Src/Lyn, and MEK/ERK. The results suggest that the migration/recruitment of monocytes and fibrocytes into fibrotic tissues, mediated at least in part by CCR1, CCR2, and CCR3, plays a major role in the progression of lung and skin fibrosis and in the predisposition of AA to fibrotic diseases. Our findings further suggest that chemokine receptors and signaling molecules, particularly caveolin-1, that control their expression/function are promising targets for treating fibrotic diseases.
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Registered trials
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