ArticleCell death & disease2015
Glycation of vitronectin inhibits VEGF-induced angiogenesis by uncoupling VEGF receptor-2-αvβ3 integrin cross-talk.
Article in Cell death & disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 28 citations in OpenAlex.
- Brazilin attenuates methylglyoxal‑induced endothelial injury by enhancing eIF5A hypusination and inhibiting the AMPK/mTOR‑mediated autophagy/apoptosis axisInternational journal of molecular medicine · 2026Article
- Enhancing the Potency of Growth Factor-Mimicking Peptides via Cross-Presentation With Integrin Ligands.Journal of biomedical materials research. Part A · 2025Article
- How Does Tendon Region, Donor, and the Presence of Disease Affect Protein Composition of the Achilles Tendon?Clinical orthopaedics and related research · 2025Article
- TCN1 Deficiency Inhibits the Malignancy of Colorectal Cancer Cells by Regulating the ITGB4 Pathway.Gut and liver · 2023Article
- Glycation of Tie-2 Inhibits Angiopoietin-1 Signaling Activation and Angiopoietin-1-Induced Angiogenesis.International journal of molecular sciences · 2022Article
- Recent Developments in the Study of the Microenvironment of Cancer and Drug Delivery.Current drug metabolism · 2022Article
- Glycation of fibronectin inhibits VEGF-induced angiogenesis by uncoupling VEGF receptor-2-c-Src crosstalk.Journal of cellular and molecular medicine · 2020Article
- The role of extracellular matrix in the pathophysiology of diabetic wounds.Matrix biology plus · 2020Article
- Review
- A Novel Role of Ascorbic Acid in Anti-Inflammatory Pathway and ROS Generation in HEMA Treated Dental Pulp Stem Cells.Materials (Basel, Switzerland) · 2019Article
- Systematic Identification of Cell-Cell Communication Networks in the Developing Brain.iScience · 2019Article
- The hypoxic tumour microenvironment.Oncogenesis · 2018Review
- Src Plays an Important Role in AGE-Induced Endothelial Cell Proliferation, Migration, and Tubulogenesis.Frontiers in physiology · 2018Article
- Integrin-β4 is a novel transcriptional target of TAp73.Cell cycle (Georgetown, Tex.) · 2018Article
- Methylglyoxal-induced glycation changes adipose tissue vascular architecture, flow and expansion, leading to insulin resistance.Scientific reports · 2017Article
- Nonenzymatic glycation interferes with fibronectin-integrin interactions in vascular smooth muscle cells.Microcirculation (New York, N.Y. : 1994) · 2017Article
- Prostaglandin EBiomedical reports · 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
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glycation of vessel wall proteins is thought to have an important role in the pathogenesis of vascular complications in diabetes mellitus. However, no previous study has implicated glycated vitronectin (VN) in the control of vascular endothelial growth factor (VEGF) signaling. To explore whether the glycation of VN affects angiogenic signaling and to understand the molecular mechanisms involved, we synthesized glycated VN by incubating VN with methylglyoxal (MGO) in vitro and identified the formation of glycated VN by an LC-ESI-MS/MS-based method. We tested the hypothesis that glycation of VN downregulates VEGF receptor-2 (VEGFR-2) activation by uncoupling the interaction between VEGFR-2 and αvβ3. Unmodified and MGO-glycated VN were used as substrates for human umbilical vein endothelial cells (HUVECs). The effects of glycated VN on VEGF signaling in HUVECs were investigated. The glycation of VN inhibited VEGF-induced phosphorylation of VEGFR-2 and the intracellular signaling pathway downstream of VEGFR-2. Glycated VN inhibited the binding of VEGFR-2 to β3 integrin and inhibited the phosphorylation of β3 integrin. Furthermore, glycation of VN significantly decreased VEGF-induced migration of HUVECs in vitro and vessel outgrowth in an ex vivo angiogenesis model. Collectively, these data indicate that the glycation of VN inhibits VEGF-induced VEGFR-2 activation by uncoupling VEGFR-2-αvβ3 integrin cross-talk. The glycation of VN causes a reduction in the migration of endothelial cells and vessel outgrowth. This may provide a mechanism for the failure of collateral sprouting in diabetic microangiopathy.
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.