ArticleJournal of translational medicine2013
VEGF-A isoform modulation in an preclinical TNBS model of ulcerative colitis: protective effects of a VEGF164b therapy.
Article in Journal of translational medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 38 citations in OpenAlex.
- IFN-γ drives inflammatory bowel disease pathogenesis through VE-cadherin-directed vascular barrier disruption.The Journal of clinical investigation · 2019Trial
- Response surface-optimized Cycas revoluta leaf extract attenuates experimental ulcerative colitis through anti-inflammatory and oxidative stress-related mechanisms.Inflammopharmacology · 2026Article
- Endothelial VEGFR-2 Activation Precedes Severe Mucosal Injury in TNBS-Induced Colitis.International journal of molecular sciences · 2026Article
- Potential for anti‑angiogenic therapy targeting the receptor for advanced glycation end products/VEGF axis in ulcerative colitis (Review).Molecular medicine reports · 2026Review
- Across Barriers: Blood-Brain and Gut Barrier Signaling in Psychiatric Disorders.Journal of neurochemistry · 2025Review
- Synthetic Antiangiogenic Vascular Endothelial Growth Factor-A Splice Variant Revascularizes Ischemic Muscle in Peripheral Artery Disease.Journal of the American Heart Association · 2024Article
- Contribution of Blood Vessel Activation, Remodeling and Barrier Function to Inflammatory Bowel Diseases.International journal of molecular sciences · 2023Review
- An assessment of vaping-induced inflammation and toxicity: A feasibility study using a 2-stage zebrafish and mouse platform.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2022Article
- To investigate the effects of artemisinin on inflammatory factors and intestinal microbiota in rats with ulcerative colitis based on network pharmacology.Frontiers in gastroenterology (Lausanne, Switzerland) · 2022Article
- Mesenchymal stem cells have ameliorative effect on the colitis model via Nrf2/HO-1 pathway.Acta cirurgica brasileira · 2022Article
- Differences in activation of intracellular signaling in primary human retinal endothelial cells between isoforms of VEGFA 165.Molecular vision · 2021Article
- Angiocrine Regulation of Epithelial Barrier Integrity in Inflammatory Bowel Disease.Frontiers in medicine · 2021Review
- Preclinical Study in Vivo for New Pharmacological Approaches in Inflammatory Bowel Disease: A Systematic Review of Chronic Model of TNBS-Induced Colitis.Journal of clinical medicine · 2019Review
- Systematic large-scale meta-analysis identifies miRNA-429/200a/b and miRNA-141/200c clusters as biomarkers for necrotizing enterocolitis in newborn.Bioscience reports · 2019Article
- Integrated in vivo multiomics analysis identifies p21-activated kinase signaling as a driver of colitis.Science signaling · 2018Article
- Pathophysiological role of guanylate-binding proteins in gastrointestinal diseases.World journal of gastroenterology · 2016Review
- Colonic Insult Impairs Lymph Flow, Increases Cellular Content of the Lymph, Alters Local Lymphatic Microenvironment, and Leads to Sustained Inflammation in the Rat Ileum.Inflammatory bowel diseases · 2015Article
- Microangiopathy triggers, and inducible nitric oxide synthase exacerbates dextran sulfate sodium-induced colitis.Laboratory investigation; a journal of technical methods and pathology · 2015Article
- Alpha-lipoic acid attenuates trinitrobenzene sulfonic acid-induced ulcerative colitis in mice.International journal of clinical and experimental medicine · 2015Article
- Angiogenesis in Inflammatory Bowel Disease.International journal of inflammation · 2015Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
backgroundUlcerative colitis (UC) is the most common form of inflammatory bowel disease in the USA. A key component of UC is the increase in inflammatory angiogenesis of the colon during active disease. This increase is driven to a great extent by the over expression of VEGF-A. Recently, VEGF165(b) (VEGF164(b) in mouse), an anti-angiogenic form of VEGF-A was described and its regulation was determined to be disturbed in many pathologies such as cancer and pre-eclampsia.
resultsThe aims of this study were to examine the role of this inhibitory VEGF by expressing this molecule in a model of intestinal inflammation, and to evaluate its expression as a potential new therapeutic approach for treating UC. A modified model of TNBS colitis was used to determine the effects of rVEGF164(b) expression on colon inflammation. Expansion of the vascular system was assessed by immunhistochemical methods and macro- and microscopic measurements of inflammation in the colon were measured. Leukocyte invasion of the tissue was measured by myeloperoxidase assay and identification and counting of lymphoid follicles. Both angio- and lymphangiogenesis were reduced by expression of rVEGF164(b), which correlated with reduction in both gross and microscopic inflammatory scores. Leukocyte invasion of the tissue was also reduced by rVEGF164(b) expression.
conclusionsThis is the first report using an endogenous inhibitory VEGF-A isoform for therapy in a model of experimental colitis. Inhibitory VEGF molecules play an important role in maintenance of gut homeostasis and may be dysregulated in UC. The results of this study suggest that restoration of rVEGF164(b) expression has anti-inflammatory activity in a TNBS model and warrants further examination as a possible therapeutic for UC.
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