ArticleDiabetologia2003
Intercellular signalling within vascular cells under high D-glucose involves free radical-triggered tyrosine kinase activation.
Article in Diabetologia, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 28 citations in OpenAlex.
- Dysregulated Erythroid MgFrontiers in cell and developmental biology · 2022Article
- Inhibition of TLR4 attenuates vascular dysfunction and oxidative stress in diabetic rats.Journal of molecular medicine (Berlin, Germany) · 2015Article
- Connexin43 mediates NF-κB signalling activation induced by high glucose in GMCs: involvement of c-Src.Cell communication and signaling : CCS · 2013Article
- Constant or fluctuating hyperglycemias increases cytomembrane stiffness of human umbilical vein endothelial cells in culture: roles of cytoskeletal rearrangement and nitric oxide synthesis.BMC cell biology · 2013Article
- Article
- Synaptopodin family of natively unfolded, actin binding proteins: physical properties and potential biological functions.Biophysical reviews · 2010Review
- High FFA-induced proliferation and apoptosis in human umbilical vein endothelial cell partly through Wnt/beta-catenin signal pathway.Molecular and cellular biochemistry · 2010Article
- Intracellular Ca2+ regulating proteins in vascular smooth muscle cells are altered with type 1 diabetes due to the direct effects of hyperglycemia.Cardiovascular diabetology · 2010Article
- Mitochondrial protein phosphorylation: instigator or target of lipotoxicity?Trends in endocrinology and metabolism: TEM · 2009Review
- Mitochondrial Ca2+, the secret behind the function of uncoupling proteins 2 and 3?Cell calcium · 2008Article
- Integrin clustering enables anandamide-induced Ca2+ signaling in endothelial cells via GPR55 by protection against CB1-receptor-triggered repression.Journal of cell science · 2008Article
- Uncoupling proteins 2 and 3 are fundamental for mitochondrial Ca2+ uniport.Nature cell biology · 2007Article
- Mechanisms underlying lysophosphatidylcholine-induced potentiation of vascular contractions in the Otsuka Long-Evans Tokushima Fatty (OLETF) rat aorta.British journal of pharmacology · 2006Article
- Mitochondria maintain maturation and secretion of lipoprotein lipase in the endoplasmic reticulum.The Biochemical journal · 2006Article
- Effect of heme and heme oxygenase-1 on vascular endothelial growth factor synthesis and angiogenic potency of human keratinocytes.Free radical biology & medicine · 2006Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisDiabetes mellitus is associated with endothelial dysfunction in human arteries due to the release of superoxide anions (*O(2)(-)) that was found to occur predominantly in smooth muscle cells (SMC). This study was designed to elucidate the impact of high glucose concentration mediated radical production in SMC on EC. Pre-treatment of vascular SMC with increased D-glucose enhanced release of *O(2)(-).
methodsMicroscope-based analyses of intracellular free Ca(2+) concentration (fura-2), immunohistochemistry (f-actin) and tyrosine kinase activity were performed. Furthermore, RT-PCR and Western blots were carried out.
resultsInteraction of EC with SMC pre-exposed to high glucose concentration yielded changes in endothelial Ca(2+) signalling and polymerization of f-actin in a concentration-dependent and superoxide dismutase (SOD) sensitive manner. This interaction activated endothelial tyrosine kinase(s) but not NFkappaB and AP-1, while SOD prevented tyrosine kinase stimulation but facilitated NFkappaB and AP-1 activation. Erbstatin, herbimycin A and the src family specific kinase inhibitor PP-1 but not the protein kinase C inhibitor GF109203X prevented changes in endothelial Ca(2+) signalling and cytoskeleton organization induced by pre-exposure of SMC to high glucose concentration. Adenovirus-mediated expression of kinase-inactive c-src blunted the effect of pre-exposure of SMC to high glucose concentration on EC. CONCLUSIONS/
interpretationThese data suggest that SMC-derived *O(2)(-) alter endothelial cytoskeleton organization and Ca(2+) signalling via activation of c-src. The activation of c-src by SMC-derived radicals is a new concept of the mechanisms underlying vascular dysfunction in diabetes.
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.