ArticlePloS one2014
Prostacyclin analogue beraprost inhibits cardiac fibroblast proliferation depending on prostacyclin receptor activation through a TGF β-Smad signal pathway.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 39 citations in OpenAlex.
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- Integration of cAMP and TRPV4 Signaling to Optimize Collagen Remodeling for Management of Fibrosis.Cells · 2025Review
- Pericardial Effusion and Prostacyclin Analog Toxicity After Initiation of Sotatercept.Pulmonary circulation · 2025Article
- ADAM17/PTGS2 Facilitates Pulmonary Fibrosis by Regulating Ferroptosis.Journal of cellular and molecular medicine · 2025Article
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- Prostanoids in Cardiac and Vascular Remodeling.Arteriosclerosis, thrombosis, and vascular biology · 2024Review
- Rhamnocitrin Attenuates Ovarian Fibrosis in Rats with Letrozole-Induced Experimental Polycystic Ovary Syndrome.Oxidative medicine and cellular longevity · 2022Article
- ST-segment resolution as a marker for severe myocardial fibrosis in ST-segment elevation myocardial infarction.BMC cardiovascular disorders · 2021Article
- The Roles of Various Prostaglandins in Fibrosis: A Review.Biomolecules · 2021Review
- Quercetin prevents myocardial infarction adverse remodeling in rats by attenuating TGF-β1/Smad3 signaling: Different mechanisms of action.Saudi journal of biological sciences · 2021Article
- RAS inhibition in resident fibroblast biology.Cellular signalling · 2021Review
- Protective Effects of Sacubitril/Valsartan on Cardiac Fibrosis and Function in Rats With Experimental Myocardial Infarction Involves Inhibition of Collagen Synthesis by Myocardial Fibroblasts Through Downregulating TGF-β1/Smads Pathway.Frontiers in pharmacology · 2021Article
- Synthetic Prostacyclin Agonist Attenuates Pressure-Overloaded Cardiac Fibrosis by Inhibiting FMT.Molecular therapy. Methods & clinical development · 2020Article
- Histomorphological, VEGF and TGF-β immunoexpression changes in the diabetic rats' ovary and the potential amelioration following treatment with metformin and insulin.Journal of molecular histology · 2020Article
- Review
- Renin cells with defective Gsα/cAMP signaling contribute to renal endothelial damage.Pflugers Archiv : European journal of physiology · 2019Article
- Effect of beraprost on pulmonary hypertension due to left ventricular systolic dysfunction.Medicine · 2019Observational
- Effects of selexipag and its active metabolite in contrasting the profibrotic myofibroblast activity in cultured scleroderma skin fibroblasts.Arthritis research & therapy · 2018Article
- DHEA-induced ovarian hyperfibrosis is mediated by TGF-β signaling pathway.Journal of ovarian research · 2018Article
- The effect of iloprost on cell proliferation and angiogenesis-related gene expression in human periodontal ligament cells.Odontology · 2018Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous studies showed that prostacyclin inhibited fibrosis. However, both receptors of prostacyclin, prostacyclin receptor (IP) and peroxisome proliferator-activated receptor (PPAR), are abundant in cardiac fibroblasts. Here we investigated which receptor was vital in the anti-fibrosis effect of prostacyclin. In addition, the possible mechanism involved in protective effects of prostacyclin against cardiac fibrosis was also studied. We found that beraprost, a prostacyclin analogue, inhibited angiotensin II (Ang II)-induced neonatal rat cardiac fibroblast proliferation in a concentration-dependent and time-dependent manner. Beraprost also suppressed Ang II-induced collagen I mRNA expression and protein synthesis in cardiac fibroblasts. After IP expression was knocked down by siRNA, Ang II-induced proliferation and collagen I synthesis could no longer be rescued by beraprost. However, treating cells with different specific inhibitors of PPAR subtypes prior to beraprost and Ang II stimulation, all of the above attenuating effects of beraprost were still available. Moreover, beraprost significantly blocked transforming growth factor β (TGF β) expression as well as Smad2 phosphorylation and reduced Smad-DNA binding activity. Beraprost also increased phosphorylation of cAMP response element binding protein (CREB) at Ser133 in the nucleus. Co-immunoprecipitation analysis revealed that beraprost increased CREB but decreased Smad2 binding to CREB-binding protein (CBP) in nucleus. In conclusion, beraprost inhibits cardiac fibroblast proliferation by activating IP and suppressing TGF β-Smad signal pathway.
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