ArticleJournal of cellular physiology2014
Heparin responses in vascular smooth muscle cells involve cGMP-dependent protein kinase (PKG).
Article in Journal of cellular physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 26 citations in OpenAlex.
- Tunable Bioresorbable Scaffolds With Marine Sulfated Polysaccharides for Small-Caliber Vascular Grafts: A Multi-Layered Strategy Combining Electrospinning and 4-Axis Printing.Advanced healthcare materials · 2026Article
- Article
- Multifaceted Heparin: Diverse Applications beyond Anticoagulant Therapy.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Involvement of transmembrane protein 184a during angiogenesis in zebrafish embryos.Frontiers in physiology · 2022Article
- Tetramethylpyrazine Improves Monocrotaline-Induced Pulmonary Hypertension through the ROS/iNOS/PKG-1 Axis.Journal of healthcare engineering · 2022Article
- Thrombolytic Agents: Nanocarriers in Controlled Release.Small (Weinheim an der Bergstrasse, Germany) · 2020Review
- Endothelial nitric oxide synthase activation is required for heparin receptor effects on vascular smooth muscle cells.American journal of physiology. Cell physiology · 2020Article
- Bioprinting of freestanding vascular grafts and the regulatory considerations for additively manufactured vascular prostheses.Translational research : the journal of laboratory and clinical medicine · 2019Review
- Heparin-Modified Collagen Gels for Controlled Release of Pleiotrophin: Potential for Vascular Applications.Frontiers in bioengineering and biotechnology · 2019Article
- Beneficial Effect of Berberis amurensis Rupr. on Penile Erection.Chinese journal of integrative medicine · 2018Article
- Pentosan polysulfate binds to STRO-1Stem cell research & therapy · 2017Article
- Using a GFP-tagged TMEM184A Construct for Confirmation of Heparin Receptor Identity.Journal of visualized experiments : JoVE · 2017Article
- Culture Medium Supplements Derived from Human Platelet and Plasma: Cell Commitment and Proliferation Support.Frontiers in bioengineering and biotechnology · 2017Article
- Novel Heparin Receptor Transmembrane Protein 184a Regulates Angiogenesis in the Adult Zebrafish Caudal Fin.Frontiers in physiology · 2017Article
- Transmembrane Protein 184A Is a Receptor Required for Vascular Smooth Muscle Cell Responses to Heparin.The Journal of biological chemistry · 2016Article
- 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
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Published data provide strong evidence that heparin treatment of proliferating vascular smooth muscle cells results in decreased signaling through the ERK pathway and decreases in cell proliferation. In addition, these changes have been shown to be mimicked by antibodies that block heparin binding to the cell surface. Here, we provide evidence that the activity of protein kinase G is required for these heparin effects. Specifically, a chemical inhibitor of protein kinase G, Rp-8-pCPT-cGMS, eliminates heparin and anti-heparin receptor antibody effects on bromodeoxyuridine incorporation into growth factor-stimulated cells. In addition, protein kinase G inhibitors decrease heparin effects on ERK activity, phosphorylation of the transcription factor Elk-1, and heparin-induced MKP-1 synthesis. Although transient, the levels of cGMP increase in heparin treated cells. Finally, knock down of protein kinase G also significantly decreases heparin effects in growth factor-activated vascular smooth muscle cells. Together, these data indicate that heparin effects on vascular smooth muscle cell proliferation depend, at least in part, on signaling through protein kinase G.
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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.