ArticleCardiovascular diabetology2010
Enhanced inflammatory responses to toll-like receptor 2/4 stimulation in type 1 diabetic coronary artery endothelial cells: the effect of insulin.
Article in Cardiovascular diabetology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 31 citations in OpenAlex.
- Impact of Type 1 Diabetes on Endothelial Cells Derived From Living Donors.FASEB bioAdvances · 2025Article
- Beyond inflammation: the multifaceted therapeutic potential of targeting the CXCL8-CXCR1/2 axis in type 1 diabetes.Frontiers in immunology · 2025Review
- Mechanism of Yi-Qi-Bu-Shen Recipe for the Treatment of Diabetic Nephropathy Complicated with Cognitive Dysfunction Based on Network Pharmacology and Experimental Validation.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Article
- AGEs-RAGE-KHeliyon · 2023Article
- The Problem of Wound Healing in Diabetes-From Molecular Pathways to the Design of an Animal Model.International journal of molecular sciences · 2022Review
- Macrophage ICAM-1 functions as a regulator of phagocytosis in LPS induced endotoxemia.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021Article
- The Mechanism of Contrast-Induced Acute Kidney Injury and Its Association with Diabetes Mellitus.Contrast media & molecular imaging · 2020Review
- Interleukin-37: The Effect of Anti-Inflammatory Response in Human Coronary Artery Endothelial Cells.Mediators of inflammation · 2019Review
- Nox2 contributes to hyperinsulinemia-induced redox imbalance and impaired vascular function.Redox biology · 2017Article
- Innate immunity in diabetes and diabetic nephropathy.Nature reviews. Nephrology · 2016Review
- Type 2 diabetes mellitus: From a metabolic disorder to an inflammatory condition.World journal of diabetes · 2015Review
- TLR2 expression doesn't change in ox-LDL mediated inflammation in Human umbilical vein endothelial cells under high glucose culture.International journal of clinical and experimental medicine · 2015Article
- Gender disparity in the role of TLR2 in post-ischemic myocardial inflammation and injury.International journal of clinical and experimental medicine · 2015Article
- The role of TLR2 and 4-mediated inflammatory pathways in endothelial cells exposed to high glucose.PloS one · 2014Article
- Postprandial hyperglycemia and endothelial function in type 2 diabetes: focus on mitiglinide.Cardiovascular diabetology · 2012Review
- Global gene expression profiling displays a network of dysregulated genes in non-atherosclerotic arterial tissue from patients with type 2 diabetes.Cardiovascular diabetology · 2012Article
- Improved Metabolic Control in Diabetes, HSP60, and Proinflammatory Mediators.Autoimmune diseases · 2012Article
- Toll-like receptor 4 promotes tubular inflammation in diabetic nephropathy.Journal of the American Society of Nephrology : JASN · 2012Article
- Toll/interleukin-1 receptor member ST2 exhibits higher soluble levels in type 2 diabetes, especially when accompanied with left ventricular diastolic dysfunction.Cardiovascular diabetology · 2011Article
- Real-time ophthalmoscopic findings of superselective intraophthalmic artery chemotherapy in a nonhuman primate model.Archives of ophthalmology (Chicago, Ill. : 1960) · 2011Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundEndothelial inflammatory responses mediated by Toll-like receptors (TLRs), particularly TLR2 and TLR4, play an important role in atherogenesis. While Type 1 diabetes (T1D) promotes the development and progression of atherosclerosis, the effect of T1D on TLR2/4-mediated inflammatory responses in coronary artery endothelial cells (CAECs) remains unclear.
methodsWe tested the hypothesis that diabetic CAECs have enhanced inflammatory responses to TLR2/4 stimulation. Non-diabetic and diabetic CAECs were treated with TLR2 agonist peptidoglycan and TLR4 agonist lipopolysaccharide. The expression of ICAM-1, IL-6 and IL-8 were analyzed by real-time PCR, immunoblotting and ELISA, and NF-κB activation by immunoblotting and immunostaining. In additional experiments, insulin was added before TLR stimulation to determine whether insulin deficiency alone is responsible for the alteration of TLR2/4-mediated inflammatory responses.
resultsStimulation of TLR2 or TLR4 induced NF-κB activation, and the expression of ICAM-1, IL-6 and IL-8. Interestingly, the expression of inflammatory mediators was significantly enhanced in diabetic cells. The enhanced inflammatory responses correlated with augmented NF-κB activation in the absence of a change in TLR2 or TLR4 protein levels. Further, pretreatment of diabetic cells with insulin failed to suppress the enhanced inflammatory responses.
conclusionsDiabetic CAECs have enhanced inflammatory responses to stimulation of TLR2 or TLR4, and insulin alone is insufficient to correct the hyper-inflammatory responses. The mechanism underlying the enhanced inflammatory responses appears to be augmentation of pro-inflammatory signaling, rather than up-regulation of levels of TLR2 and TLR4. These findings suggest that diabetic CAECs adopt a hyper-inflammatory phenotype and that this endothelial phenotypic change may predispose coronary artery to atherogenesis.
Identifiers
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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.