ArticleAmerican journal of respiratory cell and molecular biology2013
Reversal of myofibroblast differentiation by prostaglandin E(2).
Article in American journal of respiratory cell and molecular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.
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Who cites it
84 citing papers in PubMed, 125 citations in OpenAlex.
- Ginseng as a Functional Food Intervention for Interstitial Lung Disease: A Review of the Benefits and Molecular Mechanisms.Food science & nutrition · 2026Review
- MRC2-mediated collagen internalization is reduced in fibrotic lung fibroblasts and increased upon phenotypic dedifferentiation.JCI insight · 2026Article
- TGFβ primes alveolar-like macrophages to induce type I IFN following TLR2 activation.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Targeting the DNA damage repair protein RAD51 alters fibroblast metabolism and enhances apoptosis in pulmonary fibrosis.bioRxiv : the preprint server for biology · 2026Article
- Therapeutic Anti-Fibrotic Effects of a Dual Hyaluronic Acid Hybrid Complex in Bleomycin-Induced Dermal Fibrosis and UVB-Irradiated Human Skin.International journal of molecular sciences · 2026Article
- Myogenic Differentiation (MyoD) Gene Expression in Cornea and Role in Corneal Myofibroblast Dedifferentiation.Investigative ophthalmology & visual science · 2026Article
- Mechanistic basis for the antifibrotic actions of cAMP-based therapies.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- Bidirectional Interaction Between PGEProteomes · 2025Article
- Reimagining Fibrosis Research, Outcomes, and Therapeutics Through the Lens of Resolution.Seminars in respiratory and critical care medicine · 2025Review
- Distinct cAMP Regulation in Scleroderma Lung and Skin Myofibroblasts Governs Their Dedifferentiation via p38α Inhibition.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Fibroblasts in immune responses, inflammatory diseases and therapeutic implications.Nature reviews. Rheumatology · 2025Review
- Cyclic nucleotide phosphodiesterases as drug targets.Pharmacological reviews · 2025Review
- Epidermal stem cell derived exosomes-induced dedifferentiation of myofibroblasts inhibits scarring via the miR-203a-3p/PIK3CA axis.Journal of nanobiotechnology · 2025Article
- Administration of a combination of COX-2/TGF-β1 siRNAs induces hypertrophic scar fibroblast apoptosis through a TP53 mediated caspase pathway.Scientific reports · 2024Article
- Characterization of Endothelial Cell Subclusters in Localized Scleroderma Skin with Single-Cell RNA Sequencing Identifies NOTCH Signaling Pathway.International journal of molecular sciences · 2024Article
- Regulation of myofibroblast dedifferentiation in pulmonary fibrosis.Respiratory research · 2024Review
- Delivery technologies for therapeutic targeting of fibronectin in autoimmunity and fibrosis applications.Advanced drug delivery reviews · 2024Review
- MAPK phosphatase 1 inhibition of p38α within lung myofibroblasts is essential for spontaneous fibrosis resolution.The Journal of clinical investigation · 2024Article
- Cancer-associated fibroblasts undergoing neoadjuvant chemotherapy suppress rectal cancer revealed by single-cell and spatial transcriptomics.Cell reports. Medicine · 2023Article
- Prostaglandin EFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
24 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Differentiation of fibroblasts into α-smooth muscle actin (SMA)-expressing myofibroblasts represents a critical step in the pathogenesis of fibrotic disorders, and is generally regarded as irreversible. Prostaglandin E2 (PGE2) has been shown to prevent multiple aspects of fibroblast activation, including the differentiation of fibroblasts to myofibroblasts. Here, we investigated its ability to reverse this differentiated phenotype. Fetal and adult lung fibroblasts were induced to differentiate into myofibroblasts by 24-hour culture with transforming growth factor (TGF)-β1 or endothelin-1. Cells were then treated without or with PGE2 for various intervals and assessed for α-SMA expression. In the absence of PGE2 treatment, α-SMA expression induced by TGF-β1 was persistent and stable for up to 8 days. By contrast, PGE2 treatment effected a dose-dependent decrease in α-SMA and collagen I expression that was observed 2 days after PGE2 addition, peaked at 3 days, and persisted through 8 days in culture. This effect was not explained by an increase in myofibroblast apoptosis, and indeed, reintroduction of TGF-β1 2 days after addition of PGE2 prompted dedifferentiated fibroblasts to re-express α-SMA, indicating redifferentiation to myofibroblasts. This effect of PGE2 was associated with inhibition of focal adhesion kinase signaling, and a focal adhesion kinase inhibitor was also capable of reversing myofibroblast phenotype. These data unambiguously demonstrate reversal of established myofibroblast differentiation. Because many patients have established or even advanced fibrosis by the time they seek medical attention, this capacity of PGE2 has the potential to be harnessed for therapy of late-stage fibrotic disorders.
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Registered trials
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.