ArticleGlycoconjugate journal2012
Heparan sulfate expression is affected by inflammatory stimuli in primary human endothelial cells.
Article in Glycoconjugate journal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 13 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
13 citing papers in PubMed, 17 citations in OpenAlex.
- Trauma promotes heparan sulfate modifications and cleavage that disrupt homeostatic gene expression in microvascular endothelial cells.Frontiers in cell and developmental biology · 2024Article
- Extracellular sulfatase-2 is overexpressed in rheumatoid arthritis and mediates the TNF-α-induced inflammatory activation of synovial fibroblasts.Cellular & molecular immunology · 2022Article
- Heparan Sulfate Glycosaminoglycans: (Un)Expected Allies in Cancer Clinical Management.Biomolecules · 2021Review
- Review
- Review of Alterations in Perlecan-Associated Vascular Risk Factors in Dementia.International journal of molecular sciences · 2020Review
- HS and Inflammation: A Potential Playground for the Sulfs?Frontiers in immunology · 2020Review
- Loss of endothelial sulfatase-1 after experimental sepsis attenuates subsequent pulmonary inflammatory responses.American journal of physiology. Lung cellular and molecular physiology · 2019Article
- Effect of Polarization and Chronic Inflammation on Macrophage Expression of Heparan Sulfate Proteoglycans and Biosynthesis Enzymes.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2019Review
- The "in and out" of glucosamine 6-O-sulfation: the 6th sense of heparan sulfate.Glycoconjugate journal · 2017Review
- Proteoglycans in liver cancer.World journal of gastroenterology · 2016Review
- Role of the endothelial surface layer in neutrophil recruitment.Journal of leukocyte biology · 2015Review
- Article
- Glycoconjugates and related molecules in human vascular endothelial cells.International journal of vascular medicine · 2013Review
Corrections and comments
- Erratum issued
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In diabetes the endothelium is either chronically or transiently exposed to hyperglycemic conditions. In addition, endothelial dysfunction in diabetes is related to changes in the inflammatory response and the turnover of extracellular matrix. This study was undertaken to study the effects of inflammatory stimuli on one particular matrix component, the heparan sulfate (HS) proteoglycans (PGs) synthesized by primary human umbilical cord vein endothelial cells (HUVEC). Such cells were cultured in vitro in 5 mM and 25 mM glucose. The latter concentration was used to mimic hyperglycemic conditions in short-term experiments. HUVEC were also cultured in the presence of the inflammatory agents tumor necrosis factor α (TNF-α), interleukin 1α (IL-1α), interleukin 1β (IL-1β) and transforming growth factor β (TGF-β). The cells were labeled with (35)S-sulfate and (35)S-PGs were recovered for further analyses. The major part of the (35)S-PGs was secreted to the medium, irrespective of type of stimuli. Secreted (35)S-PGs were therefore isolated and subjected to further analyses. TNF-α and IL-1α slightly increased the release of (35)S-PGs to the culture medium, whereas IL-1β treatment gave a significant increase. The different treatments neither changed the ratio of (35)S-HS and (35)S-chondroitin sulfate (CS) nor the macromolecular properties of the (35)S-PGs. However, the (35)S-HS chains were slightly increased in size after TNF-α treatment, and slightly decreased after TGF-β treatment, but not affected by the other treatments. Compositional analysis of labeled disaccharides showed changes in the amount of 6-O-sulfated glucosamine residues after treatment with TNF-α, IL-1α and IL-1β. Western immunoblotting showed that major HSPGs recovered from these cells were collagen XVIII, perlecan and agrin, and that secretion of these distinct PGs was increased after IL-1β stimulation. Hence, short term inflammatory stimuli increased the release of HSPGs in HUVEC and affected both the size and sulfation pattern of HS, depending on type of stimuli.
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.