ArticleThe Journal of biological chemistry2016
Heparin Decreases in Tumor Necrosis Factor α (TNFα)-induced Endothelial Stress Responses Require Transmembrane Protein 184A and Induction of Dual Specificity Phosphatase 1.
Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 24 citations in OpenAlex.
- Patient-specific iPSC-derived ECs identify QKI-7 as a key regulator of endothelial dysfunction and potential therapeutic target in diabetes.Stem cells translational medicine · 2026Article
- Mast cell extracellular granules are bioactive condensates assembled by heparin and polyamine.Nature chemical biology · 2026Article
- TMEM184A promotes progression and drug resistance in colorectal cancer: a bioinformatics and clinical study.Scientific reports · 2026Article
- Mast cell extracellular granules are bioactive condensates driven by heparin and polyamine.bioRxiv : the preprint server for biology · 2025Article
- Cohesin protein Smc3 influences kinocilial structure and function.Biology open · 2025Article
- The SLC-ome of membrane transport: From molecular discovery to physiology and clinical applications.Physiological reviews · 2025Review
- Article
- Efficacy and predictors of immune checkpoint inhibitors in patients with gallbladder cancer.Cancer science · 2024Article
- In-depth proteomic analysis identifies key gene signatures predicting therapeutic efficacy of anti-PD-1/PD-L1 monotherapy in non-small cell lung cancer.Translational lung cancer research · 2024Article
- Epigenome-wide association of neonatal methylation and trimester-specific prenatal PMEnvironmental epidemiology (Philadelphia, Pa.) · 2022Article
- Comprehensive transcriptome profiling of urothelial cells following TNFα stimulation in anFrontiers in immunology · 2022Article
- Article
- Involvement of transmembrane protein 184a during angiogenesis in zebrafish embryos.Frontiers in physiology · 2022Article
- Prognostic Effect of Inflammatory Genes on Stage I-III Colorectal Cancer-Integrative Analysis of TCGA Data.Cancers · 2021Article
- Discovery and Validation of Novel Methylation Markers inDisease markers · 2021Article
- Endothelial nitric oxide synthase activation is required for heparin receptor effects on vascular smooth muscle cells.American journal of physiology. Cell physiology · 2020Article
- Expansion of Single Cell Transcriptomics Data of SARS-CoV Infection in Human Bronchial Epithelial Cells to COVID-19.Biological procedures online · 2020Article
- Different signaling pathways involved in the anti-inflammatory effects of unfractionated heparin on lipopolysaccharide-stimulated human endothelial cells.Journal of inflammation (London, England) · 2020Article
- Pentosan polysulfate binds to STRO-1Stem cell research & therapy · 2017Article
- Endothelial barrier protective properties of low molecular weight heparin: A novel potential tool in the prevention of cancer metastasis?Research and practice in thrombosis and haemostasis · 2017Article
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 2 institutions in 1 country.
Funding
Abstract
Despite the large number of heparin and heparan sulfate binding proteins, the molecular mechanism(s) by which heparin alters vascular cell physiology is not well understood. Studies with vascular smooth muscle cells (VSMCs) indicate a role for induction of dual specificity phosphatase 1 (DUSP1) that decreases ERK activity and results in decreased cell proliferation, which depends on specific heparin binding. The hypothesis that unfractionated heparin functions to decrease inflammatory signal transduction in endothelial cells (ECs) through heparin-induced expression of DUSP1 was tested. In addition, the expectation that the heparin response includes a decrease in cytokine-induced cytoskeletal changes was examined. Heparin pretreatment of ECs resulted in decreased TNFα-induced JNK and p38 activity and downstream target phosphorylation, as identified through Western blotting and immunofluorescence microscopy. Through knockdown strategies, the importance of heparin-induced DUSP1 expression in these effects was confirmed. Quantitative fluorescence microscopy indicated that heparin treatment of ECs reduced TNFα-induced increases in stress fibers. Monoclonal antibodies that mimic heparin-induced changes in VSMCs were employed to support the hypothesis that heparin was functioning through interactions with a receptor. Knockdown of transmembrane protein 184A (TMEM184A) confirmed its involvement in heparin-induced signaling as seen in VSMCs. Therefore, TMEM184A functions as a heparin receptor and mediates anti-inflammatory responses of ECs involving decreased JNK and p38 activity.
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.