ArticleJournal of translational medicine2018
Integrin ανβ5 in vitro inhibition limits pro-fibrotic response in cardiac fibroblasts of spontaneously hypertensive rats.
Article in Journal of translational medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 32 citations in OpenAlex.
- MiR-145-5p modulates collagen production and fibroblast behaviour after cardiac injury partially via COL5A1.Basic research in cardiology · 2026Article
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- Role of the integrin‑β1/TGF‑β1 signaling pathway in the pathogenesis of pelvic organ prolapse: A study on vaginal wall tissue alterations and molecular dysfunction.Molecular medicine reports · 2025Article
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- Roles of Integrin in Cardiovascular Diseases: From Basic Research to Clinical Implications.International journal of molecular sciences · 2024Review
- Atrial Proteomic Profiling Reveals a Switch Towards Profibrotic Gene Expression Program in CREM-IbΔC-X Mice with Persistent Atrial Fibrillation.bioRxiv : the preprint server for biology · 2024Article
- Exploiting the anti-fibrotic effects of statins on thoracic aortic aneurysm progression: results from a meta-analysis and experimental data.Frontiers in pharmacology · 2024Article
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- The Emerging Role of Cell Adhesion Molecules on Benign Prostatic Hyperplasia.International journal of molecular sciences · 2023Review
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- How Effective Is a Late-Onset Antihypertensive Treatment? Studies with Captopril as Monotherapy and in Combination with Nifedipine in Old Spontaneously Hypertensive Rats.Biomedicines · 2022Article
- Key Roles of RGD-Recognizing Integrins During Cardiac Development, on Cardiac Cells, and After Myocardial Infarction.Journal of cardiovascular translational research · 2022Review
- Transcriptome and proteome profiling of activated cardiac fibroblasts supports target prioritization in cardiac fibrosis.Frontiers in cardiovascular medicine · 2022Article
- Antihypertensive and cardioprotective effects of different monotherapies and combination therapies in young spontaneously hypertensive rats - A pilot study.Saudi journal of biological sciences · 2022Article
- Cardiac Biomarkers and Autoantibodies in Endurance Athletes: Potential Similarities with Arrhythmogenic Cardiomyopathy Pathogenic Mechanisms.International journal of molecular sciences · 2021Review
- Review
- Excess TGF-β1 Drives Cardiac Mesenchymal Stromal Cells to a Pro-Fibrotic Commitment in Arrhythmogenic Cardiomyopathy.International journal of molecular sciences · 2021Article
- Cooperative signaling between integrins and growth factor receptors in fibrosis.Journal of molecular medicine (Berlin, Germany) · 2021Review
- Potential Role of Integrin α₅β₁/Focal Adhesion Kinase (FAK) and Actin Cytoskeleton in the Mechanotransduction and Response of Human Gingival Fibroblasts Cultured on a 3-Dimension Lactide-Co-Glycolide (3D PLGA) Scaffold.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- CaMKII Activity in the Inflammatory Response of Cardiac Diseases.International journal of molecular sciences · 2019Review
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTo date the TGF-β1 activation mediated by integrin ανβ5 during fibrosis is well-known. This process has been shown also in the heart, where cardiac fibroblasts (CF) differentiate into α-smooth muscle actin (α-SMA)-positive myofibroblasts (MyoFB). Here, we studied the effects on CF, isolated by spontaneously hypertensive rats (SHR), of integrin ανβ5 inhibition in MyoFB differentiation.
methodsStaining and immunohistochemistry were performed on rat cardiac tissue. CF were isolated by enzymatic digestion from SHR (SHR-CF) and normotensive WKY (WKY-CF) rat hearts and then treated for in vitro evaluation.
resultsSHR heart tissues revealed a higher TGF-β1 expression vs. WKY samples. SHR-CF showed an enhanced SMAD2/3 activation and an up-regulated expression of α-SMA, a typical MyoFB marker, especially after TGF-β1 treatment. Immunostaining on cardiac tissues revealed a higher expression of integrin ανβ5 in SHR vs. WKY rat hearts. In vitro results confirmed the up-regulation of integrin ανβ5 expression in SHR-CF at basal condition and after TGF-β1 treatment, in comparison with WKY-CF. Inhibition of integrin ανβ5 by cilengitide treatment led a decreased expression of ανβ5, collagen I, and α-SMA in SHR-CF vs. WKY-CF, resulting in a diminished differentiation of CF into MyoFB. Taking together, results suggested that SHR-CF are more susceptible to TGF-β1, showing an up-regulated activation of SMAD2/3 signaling, and an increased ανβ5, α-SMA, and collagen I expression. Hypertension stimulus promoted an up-regulation of integrin ανβ5 on SHR cardiac tissue and its in vitro inhibition reverted pro-fibrotic events of SHR-CF.
conclusionInhibition of integrin ανβ5 exerted by cilengitide strongly diminished SHR-CF differentiation into detrimental MyoFB. So, integrin ανβ5 might be considered a novel therapeutic target and cilengitide an effective pharmacological tool to limit the progression of hypertension-induced cardiac fibrosis.
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