ArticleAmerican journal of physiology. Lung cellular and molecular physiology2010
Fibroblast-specific expression of AC6 enhances beta-adrenergic and prostacyclin signaling and blunts bleomycin-induced pulmonary fibrosis.
Article in American journal of physiology. Lung cellular and molecular physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 23 citations in OpenAlex.
- Integration of cAMP and TRPV4 Signaling to Optimize Collagen Remodeling for Management of Fibrosis.Cells · 2025Review
- The differential effects of cAMP mobilizing agents on TGF-β-induced extracellular matrix in human lung-derived fibroblasts: insights into therapeutic targets for lung fibrosis.Respiratory research · 2025Article
- Emerging Concepts in Therapeutic Interventions for Idiopathic Pulmonary Fibrosis.Seminars in respiratory and critical care medicine · 2025Review
- Prostacyclin enlists AC6 to stop the clot.Journal of thrombosis and haemostasis : JTH · 2025Article
- Recent progress in exosomal non-coding RNAs research related to idiopathic pulmonary fibrosis.Frontiers in genetics · 2025Review
- Optimized New Shengmai Powder modulation of cAMP/Rap1A signaling pathway attenuates myocardial fibrosis in heart failure.Chinese medicine · 2024Article
- Agonist-specific desensitization of PGENaunyn-Schmiedeberg's archives of pharmacology · 2020Article
- Glucocorticoids rapidly activate cAMP production via GFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Activation of the prostaglandin EActa physiologica (Oxford, England) · 2019Article
- Hydrogel scaffolds as in vitro models to study fibroblast activation in wound healing and disease.Biomaterials science · 2014Article
- Inhibition of TRPM7 channels prevents proliferation and differentiation of human lung fibroblasts.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2013Article
- Heart failure gene therapy: the path to clinical practice.Circulation research · 2013Review
- cAMP and Epac in the regulation of tissue fibrosis.British journal of pharmacology · 2012Review
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Authors and funding
7 authors at 1 institution in 1 country.
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Abstract
Pulmonary fibroblasts regulate extracellular matrix production and degradation and are critical in maintenance of lung structure, function, and repair, but they also play a central role in lung fibrosis. cAMP-elevating agents inhibit cytokine- and growth factor-stimulated myofibroblast differentiation and collagen synthesis in pulmonary fibroblasts. In the present study, we overexpressed adenylyl cyclase 6 (AC6) in pulmonary fibroblasts and measured cAMP production and collagen synthesis. AC6 overexpression enhanced cAMP production and the inhibition of collagen synthesis mediated by isoproterenol and beraprost, but not the responses to butaprost or PGE(2). To examine if increased AC6 expression would impact the development of fibrosis in an animal model, we generated transgenic mice that overexpress AC6 under a fibroblast-specific promoter, FTS1. Lung fibrosis was induced in FTS1-AC6(+/-) mice and littermate controls by intratracheal instillation of saline or bleomycin. Wild-type mice treated with bleomycin showed extensive peribronchial and interstitial fibrosis and collagen deposition. By contrast, FTS1-AC6(+/-) mice displayed decreased fibrotic development, lymphocyte infiltration (as determined by pathological scoring), and lung collagen content. Thus, AC6 overexpression inhibits fibrogenesis in the lung by reducing pulmonary fibroblast-mediated collagen synthesis and myofibroblast differentiation. Because AC6 overexpression does not lead to enhanced basal or PGE(2)-stimulated levels of cAMP, we conclude that endogenous catecholamines or prostacyclin is produced during bleomycin-induced lung fibrosis and that these signals have antifibrotic potential.
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