ArticleProceedings of the National Academy of Sciences of the United States of America2012
Epistatic interactions between Tgfb1 and genetic loci, Tgfbm2 and Tgfbm3, determine susceptibility to an asthmatic stimulus.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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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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
5 citing papers in PubMed, 13 citations in OpenAlex.
- TGFβ biology in cancer progression and immunotherapy.Nature reviews. Clinical oncology · 2021Review
- Switching Roles of TGF-β in Cancer Development: Implications for Therapeutic Target and Biomarker Studies.Journal of clinical medicine · 2016Review
- Meeting report - TGF-β superfamily: signaling in development and disease.Journal of cell science · 2013Article
- Sequencing studies in human genetics: design and interpretation.Nature reviews. Genetics · 2013Review
- Targeting the TGFβ signalling pathway in disease.Nature reviews. Drug discovery · 2012Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
TGFβ activation and signaling have been extensively studied in experimental models of allergen-induced asthma as potential therapeutic targets during chronic or acute phases of the disease. Outcomes of experimental manipulation of TGFβ activity have been variable, in part due to use of different model systems. Using an ovalbumin (OVA)-induced mouse model of asthma, we here show that innate variation within TGFβ1 genetic modifier loci, Tgfbm2 and Tgfbm3, alters disease susceptibility. Specifically, Tgfbm2(129) and Tgfbm3(C57) synergize to reverse accentuated airway hyperresponsiveness (AHR) caused by low TGFβ1 levels in Tgfb1(+/-) mice of the NIH/OlaHsd strain. Moreover, epistatic interaction between Tgfbm2(129) and Tgfbm3(C57) uncouples the inflammatory response to ovalbumin from those of airway remodeling and airway hyperresponsiveness, illustrating independent genetic control of these responses. We conclude that differential inheritance of genetic variants of Tgfbm genes alters biological responses to reduced TGFβ1 signaling in an experimental asthma model. TGFβ antagonists for treatment of lung diseases might therefore give diverse outcomes, dependent on genetic variation.
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Registered trials
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