ArticleAmerican journal of physiology. Lung cellular and molecular physiology2013
Regulation of myofibroblast differentiation and bleomycin-induced pulmonary fibrosis by adrenomedullin.
Article in American journal of physiology. Lung cellular and molecular physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 25 citations in OpenAlex.
- PUM2 knockdown regulates the expression and alternative splicing of genes associated with myocardial fibrosis in H9C2 cells.Experimental and therapeutic medicine · 2026Article
- Gα12 and Gα13 proteins are required for transforming growth factor-β-induced myofibroblast differentiation.The Biochemical journal · 2024Article
- Critical role of Gα12 and Gα13 proteins in TGF-β-induced myofibroblast differentiation.bioRxiv : the preprint server for biology · 2024Article
- Translational studies of adrenomedullin and related peptides regarding cardiovascular diseases.Hypertension research : official journal of the Japanese Society of Hypertension · 2022Review
- GPCR-mediated YAP/TAZ inactivation in fibroblasts via EPAC1/2, RAP2C, and MAP4K7.Journal of cellular physiology · 2021Article
- Expression of serum response factor in the lung mesenchyme is essential for development of pulmonary fibrosis.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- Adrenomedullin Attenuates Inflammation in White Adipose Tissue of Obese Rats Through Receptor-Mediated PKA Pathway.Obesity (Silver Spring, Md.) · 2021Article
- Extracellular CIRP Induces an Inflammatory Phenotype in Pulmonary FibroblastsFrontiers in immunology · 2021Article
- Article
- Targeting GPCR Signaling for Idiopathic Pulmonary Fibrosis Therapies.Trends in pharmacological sciences · 2020Review
- Anti-fibrotic effects of tannic acid through regulation of a sustained TGF-beta receptor signaling.Respiratory research · 2019Article
- Dibutyryl-cAMP attenuates pulmonary fibrosis by blocking myofibroblast differentiation via PKA/CREB/CBP signaling in rats with silicosis.Respiratory research · 2017Article
- Regulation of myofibroblast differentiation by cardiac glycosides.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- Downregulation of TGF-β Receptor-2 Expression and Signaling through Inhibition of Na/K-ATPase.PloS one · 2016Article
- Involvement of collagen-binding heat shock protein 47 in scleroderma-associated fibrosis.Protein & cell · 2015Article
- Megakaryoblastic leukemia-1 is required for the development of bleomycin-induced pulmonary fibrosis.Respiratory research · 2015Article
- A critical review of the American Journal of Physiology-Lung Cellular and Molecular Physiology: 2012-2015.American journal of physiology. Lung cellular and molecular physiology · 2014Review
- Antifibrotic effects of noscapine through activation of prostaglandin E2 receptors and protein kinase A.The Journal of biological chemistry · 2014Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
Myofibroblast differentiation induced by transforming growth factor-β (TGF-β) is characterized by the expression of smooth muscle α-actin (SMA) and extracellular matrix proteins. We and others have previously shown that these changes are regulated by protein kinase A (PKA). Adrenomedullin (ADM) is a vasodilator peptide that activates cAMP/PKA signaling through the calcitonin-receptor-like receptor (CRLR) and receptor-activity-modifying proteins (RAMP). In this study, we found that recombinant ADM had little effect on cAMP/PKA in quiescent human pulmonary fibroblasts, whereas it induced a profound activation of cAMP/PKA signaling in differentiated (by TGF-β) myofibroblasts. In contrast, the prostacyclin agonist iloprost was equally effective at activating PKA in both quiescent fibroblasts and differentiated myofibroblasts. TGF-β stimulated a profound expression of CRLR with a time course that mirrored the increased PKA responses to ADM. The TGF-β receptor kinase inhibitor SB431542 abolished expression of CRLR and attenuated the PKA responses of cells to ADM but not to iloprost. CRLR expression was also dramatically increased in lungs from bleomycin-treated mice. Functionally, ADM did not affect initial differentiation of quiescent fibroblasts in response to TGF-β but significantly attenuated the expression of SMA, collagen-1, and fibronectin in pre-differentiated myofibroblasts, which was accompanied by decreased contractility of myofibroblasts. Finally, sensitization of ADM signaling by transgenic overexpression of RAMP2 in myofibroblasts resulted in enhanced survival and reduced pulmonary fibrosis in the bleomycin model of the disease. In conclusion, differentiated pulmonary myofibroblasts gain responsiveness to ADM via increased CRLR expression, suggesting the possibility of using ADM for targeting pathological myofibroblasts without affecting normal fibroblasts.
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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.