ArticleDiabetes2011
Role of inflammation and insulin resistance in endothelial progenitor cell dysfunction.
Article in Diabetes, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 72 citations in OpenAlex.
- Association between the C-reactive protein-triglyceride glucose index and erectile dysfunction in US males: results from NHANES 2001-2004.International journal of impotence research · 2025Article
- α7nAChR Activation Combined with Endothelial Progenitor Cell Transplantation Attenuates Lung Injury in Diabetic Rats with Sepsis through the NF-κB Pathway.Inflammation · 2024Article
- IL-10 promotes endothelial progenitor cell infiltration and wound healing via STAT3.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- Salvianic Acid A Regulates High-Glucose-Treated Endothelial Progenitor Cell Dysfunction via the AKT/Endothelial Nitric Oxide Synthase (eNOS) Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2021Article
- Differential MicroRNA Expression Pattern in Endothelial Progenitor Cells During Diabetic Retinopathy.Frontiers in cell and developmental biology · 2021Article
- Review
- Article
- Interleukin-10 Deficiency Alters Endothelial Progenitor Cell-Derived Exosome Reparative Effect on Myocardial Repair via Integrin-Linked Kinase Enrichment.Circulation research · 2020Article
- A Protective Effect of PPARα in Endothelial Progenitor Cells Through Regulating Metabolism.Diabetes · 2019Article
- microRNA-21-5p dysregulation in exosomes derived from heart failure patients impairs regenerative potential.The Journal of clinical investigation · 2019Article
- Article
- Rosiglitazone accelerates wound healing by improving endothelial precursor cell function and angiogenesis inPeerJ · 2019Article
- Polysaccharide peptide (PsP) GVascular health and risk management · 2019Article
- Interleukin-10 Deficiency Impairs Reparative Properties of Bone Marrow-Derived Endothelial Progenitor Cell Exosomes.Tissue engineering. Part A · 2017Article
- Transplantation of IL-10-transfected endothelial progenitor cells improves retinal vascular repair via suppressing inflammation in diabetic rats.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2016Article
- Glucose and acute exercise influence factors secreted by circulating angiogenic cells in vitro.Physiological reports · 2016Article
- Insights into the molecular mechanisms of diabetes-induced endothelial dysfunction: focus on oxidative stress and endothelial progenitor cells.Endocrine · 2015Article
- Endothelial progenitor cells in ischemic stroke: an exploration from hypothesis to therapy.Journal of hematology & oncology · 2015Review
- Therapeutic efficacy of bone marrow-derived mononuclear cells in diabetic polyneuropathy is impaired with aging or diabetes.Journal of diabetes investigation · 2015Article
- Diabetes, Endothelial Dysfunction, and Vascular Repair: What Should a Diabetologist Keep His Eye on?International journal of endocrinology · 2015Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveEndothelial progenitor cells (EPCs) are decreased in number and function in type 2 diabetes. Mechanisms by which this dysfunction occurs are largely unknown. We tested the hypothesis that a chronic inflammatory environment leads to insulin signaling defects in EPCs and thereby reduces their survival. Modifying EPCs by a knockdown of nuclear factor-κB (NF-κB) can reverse the insulin signaling defects, improve EPC survival, and decrease neointimal hyperplasia in Zucker fatty rats postangioplasty. RESEARCH DESIGN AND
methodsEPCs from Zucker fatty insulin-resistant rats were cultured and exposed to tumor necrosis factor-α (TNF-α). Insulin signaling defects and apoptosis were measured in the presence and absence of an NF-κB inhibitor, BAY11. Then, EPCs were modified by a knockdown of NF-κB (RelA) and exposed to TNF-α. For in vivo experiments, Zucker fatty rats were given modified EPCs post-carotid angioplasty. Tracking of EPCs was done at various time points, and neointimal hyperplasia was measured 3 weeks later.
resultsInsulin signaling as measured by the phosphorylated-to-total AKT ratio was reduced by 56% in EPCs exposed to TNF-α. Apoptosis was increased by 71%. These defects were reversed by pretreatment with an NF-κB inhibitor, BAY11. Modified EPCs exposed to TNF-α showed a lesser reduction (RelA 20%) in insulin-stimulated AKT phosphorylation versus a 55% reduction in unmodified EPCs. Apoptosis was 41% decreased for RelA knockdown EPCs. Noeintimal hyperplasia postangioplasty was significantly less in rats receiving modified EPCs than in controls (intima-to-media ratio 0.58 vs. 1.62).
conclusionsIn conclusion, we have shown that insulin signaling and EPC survival is impaired in Zucker fatty insulin resistant rats. For the first time, we have shown that this defect can be significantly ameliorated by a knockdown of NF-κB and that these EPCs given to Zucker fatty rats decrease neointimal hyperplasia post-carotid angioplasty.
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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.