ArticleInternational journal of molecular sciences2013
Carbon nanotube-induced pulmonary granulomatous disease: Twist1 and alveolar macrophage M1 activation.
Article in International journal of molecular sciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 29 citations in OpenAlex.
- Single cell transcriptome signatures and cell-cell interactions associated with sarcoidosis in lung immune cell populations.Frontiers in immunology · 2026Article
- Review
- Pulmonary Sarcoidosis: Experimental Models and Perspectives of Molecular Diagnostics Using Quantum Dots.International journal of molecular sciences · 2023Review
- A transcriptomics-based meta-analysis identifies a cross-tissue signature for sarcoidosis.Frontiers in medicine · 2022Article
- Myeloid ABCG1 Deficiency Enhances Apoptosis and Initiates Efferocytosis in Bronchoalveolar Lavage Cells of Murine Multi-Walled Carbon Nanotube-Induced Granuloma Model.International journal of molecular sciences · 2021Article
- Studies in a Murine Granuloma Model of Instilled Carbon Nanotubes: Relevance to Sarcoidosis.International journal of molecular sciences · 2021Review
- Models Contribution to the Understanding of Sarcoidosis Pathogenesis: "Are There Good Models of Sarcoidosis?"Journal of clinical medicine · 2020Review
- Matrix Metalloproteinase-12 Is Required for Granuloma Progression.Frontiers in immunology · 2020Article
- Environmental Risk Factors for Sarcoidosis.Frontiers in immunology · 2020Review
- Alveolar Macrophage ABCG1 Deficiency Promotes Pulmonary Granulomatous Inflammation.American journal of respiratory cell and molecular biology · 2019Article
- PPAR-gamma pathways attenuate pulmonary granuloma formation in a carbon nanotube induced murine model of sarcoidosis.Biochemical and biophysical research communications · 2018Article
- Mechanisms of carbon nanotube-induced pulmonary fibrosis: a physicochemical characteristic perspective.Wiley interdisciplinary reviews. Nanomedicine and nanobiotechnology · 2018Review
- Transcriptional survey of alveolar macrophages in a murine model of chronic granulomatous inflammation reveals common themes with human sarcoidosis.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- Transcriptome profiles in sarcoidosis and their potential role in disease prediction.Current opinion in pulmonary medicine · 2017Review
- Multiwalled carbon nanotubes intratracheally instilled into the rat lung induce development of pleural malignant mesothelioma and lung tumors.Cancer science · 2016Article
- Exposure to a Mycobacterial Antigen, ESAT-6, Exacerbates Granulomatous and Fibrotic Changes in a Multiwall Carbon Nanotube Model of Chronic Pulmonary Disease.Journal of nanomedicine & nanotechnology · 2015Article
- Etiologies of Sarcoidosis.Clinical reviews in allergy & immunology · 2015Review
- Identification of reference genes in human myelomonocytic cells for gene expression studies in altered gravity.BioMed research international · 2015Article
- Carbon Nanotubes and Chronic Granulomatous Disease.Nanomaterials (Basel, Switzerland) · 2014Article
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9 authors at 1 institution in 1 country.
Funding
Abstract
Sarcoidosis, a chronic granulomatous disease of unknown cause, has been linked to several environmental risk factors, among which are some that may favor carbon nanotube formation. Using gene array data, we initially observed that bronchoalveolar lavage (BAL) cells from sarcoidosis patients displayed elevated mRNA of the transcription factor, Twist1, among many M1-associated genes compared to healthy controls. Based on this observation we hypothesized that Twist1 mRNA and protein expression might become elevated in alveolar macrophages from animals bearing granulomas induced by carbon nanotube instillation. To address this hypothesis, wild-type and macrophage-specific peroxisome proliferator-activated receptor gamma (PPARγ) knock out mice were given oropharyngeal instillation of multiwall carbon nanotubes (MWCNT). BAL cells obtained 60 days later exhibited significantly elevated Twist1 mRNA expression in granuloma-bearing wild-type or PPARγ knock out alveolar macrophages compared to sham controls. Overall, Twist1 expression levels in PPARγ knock out mice were higher than those of wild-type. Concurrently, BAL cells obtained from sarcoidosis patients and healthy controls validated gene array data: qPCR and protein analysis showed significantly elevated Twist1 in sarcoidosis compared to healthy controls. In vitro studies of alveolar macrophages from healthy controls indicated that Twist1 was inducible by classical (M1) macrophage activation stimuli (LPS, TNFα) but not by IL-4, an inducer of alternative (M2) macrophage activation. Findings suggest that Twist1 represents a PPARγ-sensitive alveolar macrophage M1 biomarker which is induced by inflammatory granulomatous disease in the MWCNT model and in human sarcoidosis.
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