ArticleMolecular and cellular biochemistry2014
Thrombin stimulates VSMC proliferation through an EGFR-dependent pathway: involvement of MMP-2.
Article in Molecular and cellular biochemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 17 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 30 citations in OpenAlex.
- Protease-activated receptors in vascular smooth muscle cells: a bridge between thrombo-inflammation and vascular remodelling.Cell communication and signaling : CCS · 2025Review
- Multistep Approach Points to Compounds Responsible for the Biological Activity and Safety of Hydrolates from NineAntioxidants (Basel, Switzerland) · 2023Article
- The Compatibility of Alisma and Atractylodes Affects the Biological Behaviours of VSMCs by Inhibiting the miR-128-5p/p21 Gene.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Baicalin Alleviates Thrombin-Induced Inflammation in Vascular Smooth Muscle Cells.BioMed research international · 2022Article
- Matrix Metalloproteinases and Arterial Hypertension: Role of Oxidative Stress and Nitric Oxide in Vascular Functional and Structural Alterations.Biomolecules · 2021Review
- miR-30b-5p Downregulation as a Predictive Biomarker of Coronary In-Stent Restenosis.Biomedicines · 2021Article
- Unique Angiogenesis From Cardiac Arterioles During Pericardial Adhesion Formation.Frontiers in cardiovascular medicine · 2021Article
- Role of Extracellular Matrix in Pathophysiology of Patent Ductus Arteriosus: Emphasis on Vascular Remodeling.International journal of molecular sciences · 2020Review
- Article
- Proliferation of Vascular Smooth Muscle Cells under ox-LDL Is Regulated byEvidence-based complementary and alternative medicine : eCAM · 2020Article
- Mechanisms of PAR-1 mediated kinase receptor transactivation: Smad linker region phosphorylation.Journal of cell communication and signaling · 2019Article
- COL6A1 knockdown suppresses cell proliferation and migration in human aortic vascular smooth muscle cells.Experimental and therapeutic medicine · 2019Article
- Matrix metalloproteinase-2-induced epidermal growth factor receptor transactivation impairs redox balance in vascular smooth muscle cells and facilitates vascular contraction.Redox biology · 2018Article
- EGFR is a pivotal regulator of thrombin-mediated inflammation in primary human nucleus pulposus culture.Scientific reports · 2017Article
- Article
- Wnt signaling contributes to vascular calcification by induction of matrix metalloproteinases.BMC cardiovascular disorders · 2016Article
- Article
Corrections and comments
- Retracted
Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In this study, the role of epidermal growth factor receptor (EGFR), extracellular signal-regulated kinase (ERK1/2), heparin-binding EGF-like growth factor (HB-EGF), general metalloproteinases, matrix metalloproteinases-2 (MMP-2) in mediating the mitogenic action of thrombin in rat vascular smooth muscle cells (VSMC) was investigated. The incubation of rat VSMC with thrombin (1 U/ml) for 5 min resulted in significant (p < 0.001) increase of ERK1/2 phosphorylation by 8.7 ± 0.9-fold, EGFR phosphorylation by 8.5 ± 1.3-fold (p < 0.001) and DNA synthesis by 3.6 ± 0.4-fold (p < 0.001). Separate 30-min pretreatments with EGFR tyrosine kinase irreversible inhibitor, 10 µM PD169540 (PD), and 20 µM anti-HB-EGF antibody significantly reduced thrombin-stimulated EGFR and ERK1/2 phosphorylation by 81, 72 % and by 48 and 61 %, respectively. Furthermore, the same pretreatments with PD or anti-HB-EGF antibody reduced thrombin-induced VSMC proliferation by 44 and 45 %, respectively. In addition, 30-min pretreatments with 10 µM specific MMP-2 inhibitor significantly reduced thrombin-stimulated phosphorylation of both EGFR and ERK1/2 by 25 %. Moreover, the same pretreatment with MMP-2 inhibitor reduced thrombin-induced VSMC proliferation by 45 %. These results show that the thrombin-induced DNA synthesis correlates with the level of ERK1/2 activation rather than EGFR activation. These results further suggest that thrombin acts through EGFR and ERK 1/2 signaling pathways involving MMP-2 to upregulate proliferation of VSMC.
Indexed as
Identifiers
What OpenQuestion holds
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.