ArticleBritish journal of pharmacology2001
Thrombin-induced p38 mitogen-activated protein kinase activation is mediated by epidermal growth factor receptor transactivation pathway.
Article in British journal of pharmacology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 51 citations in OpenAlex.
- Protease-activated receptors in health and disease.Physiological reviews · 2023Review
- Combined targeting of G protein-coupled receptor and EGF receptor signaling overcomes resistance to PI3K pathway inhibitors in PTEN-null triple negative breast cancer.EMBO molecular medicine · 2020Article
- Epidermal Growth Factor (EGF) Autocrine Activation of Human Platelets Promotes EGF Receptor-Dependent Oral Squamous Cell Carcinoma Invasion, Migration, and Epithelial Mesenchymal Transition.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Advanced glycation end products induce brain-derived neurotrophic factor release from human platelets through the Src-family kinase activation.Cardiovascular diabetology · 2017Article
- Thrombin stimulates VSMC proliferation through an EGFR-dependent pathway: involvement of MMP-2.Molecular and cellular biochemistry · 2014Article
- The epidermal growth factor receptor and its ligands in cardiovascular disease.International journal of molecular sciences · 2013Review
- Protease activated receptor-1 inhibits the Maspin tumor-suppressor gene to determine the melanoma metastatic phenotype.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- A differential role for endocytosis in receptor-mediated activation of Nox1.Antioxidants & redox signaling · 2010Article
- Adrenaline increases glucose transport via a Rap1-p38MAPK pathway in rat vascular smooth muscle cells.British journal of pharmacology · 2007Article
- Thrombin-induced glucose transport via Src-p38 MAPK pathway in vascular smooth muscle cells.British journal of pharmacology · 2005Article
- Ras activation in response to lysophosphatidic acid requires a permissive input from the epidermal growth factor receptor.The Biochemical journal · 2003Article
- Stimulation of beta(3)-adrenoceptors causes phosphorylation of p38 mitogen-activated protein kinase via a stimulatory G protein-dependent pathway in 3T3-L1 adipocytes.British journal of pharmacology · 2002Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Thrombin is a potent mitogen for vascular smooth muscle cells (VSMC) and has been implicated its pathogenic role in vascular remodelling. However, the signalling pathways by which thrombin mediates its mitogenic response are not fully understood. We have previously reported that thrombin activates p38 mitogen-activated protein kinase (p38 MAPK) by a tyrosine kinase-dependent mechanism, and that p38 MAPK has a role in thrombin-induced mitogenic response in rat VSMC. In the present study, we examine the involvement of epidermal growth factor (EGF) receptor in thrombin-induced p38 MAPK activation. We found that thrombin induced EGF receptor tyrosine phosphorylation (transactivation) in A10 cells, a clonal VSMC cell line. A selective inhibitor of EGF receptor kinase (AG1478) inhibited the p38 MAPK activation in a dose-dependent manner, whereas it had no effect on the response to platelet-derived growth factor (PDGF). EGF receptor phosphorylation induced by thrombin was inhibited by BAPTA-AM and GF109203X, which suggest a requirement for intracellular Ca(2+) increase and protein kinase C. We next examined the effect of AG1478 on thrombin-induced DNA synthesis. AG1478 inhibited thrombin-induced DNA synthesis in a dose-dependent manner. In contrast, PDGF-induced DNA synthesis was not affected by AG1478. In conclusion, these data suggest that the EGF receptor transactivation and subsequent p38 MAPK activation is required for thrombin-induced proliferation of VSMC.
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