ArticleJournal of cellular biochemistry2010
Heparin treatment of vascular smooth muscle cells results in the synthesis of the dual-specificity phosphatase MKP-1.
Article in Journal of cellular biochemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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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.
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Who cites it
6 citing papers in PubMed, 13 citations in OpenAlex.
- Article
- Novel Heparin Receptor Transmembrane Protein 184a Regulates Angiogenesis in the Adult Zebrafish Caudal Fin.Frontiers in physiology · 2017Article
- Heparin Decreases in Tumor Necrosis Factor α (TNFα)-induced Endothelial Stress Responses Require Transmembrane Protein 184A and Induction of Dual Specificity Phosphatase 1.The Journal of biological chemistry · 2016Article
- Transmembrane Protein 184A Is a Receptor Required for Vascular Smooth Muscle Cell Responses to Heparin.The Journal of biological chemistry · 2016Article
- Heparin responses in vascular smooth muscle cells involve cGMP-dependent protein kinase (PKG).Journal of cellular physiology · 2014Article
- Enhancing angiogenesis alleviates hypoxia and improves engraftment of enteric cells in polycaprolactone scaffolds.Journal of tissue engineering and regenerative medicine · 2013Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The ability of heparin to block proliferation of vascular smooth muscle cells has been well documented. It is clear that heparin treatment can decrease the level of ERK activity in vascular smooth muscle cells that are sensitive to heparin. In this study, the mechanism by which heparin induces decreases in ERK activity was investigated by evaluating the dual specificity phosphatase, MKP-1, in heparin treated cells. Heparin induced MKP-1 synthesis in a time and concentration dependent manner. The time-course of MKP-1 expression correlated with the decrease in ERK activity. Over the same time frame, heparin treatment did not result in decreases in MEK-1 activity which could have, along with constitutive phosphatase activity, accounted for the decrease in ERK activity. Antibodies against a heparin receptor also induced the synthesis of MKP-1 along with decreasing ERK activity. Blocking either phosphatase activity or synthesis also blocked heparin-induced decreases in ERK activity. Consistent with a role for MKP-1, a nuclear phosphatase, heparin treated cells exhibited decreases in nuclear ERK activity more rapidly than cells not treated with heparin. The data support MKP-1 as a heparin-induced phosphatase that dephosphorylates ERK, decreasing ERK activity, in vascular smooth muscle cells.
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Registered trials
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