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Long-term type 1 diabetes influences haematopoietic stem cells by reducing vascular repair potential and increasing inflammatory monocyte generation in a murine model

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TLDR
The BM microenvironment of type 1 diabetic mice can lead to changes in haematopoiesis, with generation of more monocytes and fewer EPCs contributing to development of microvascular complications and inhibition of GP130 activation may serve as a therapeutic strategy to improve the key aspects of this dysfunction.
Abstract
Aims/hypothesis We sought to determine the impact of long-standing type 1 diabetes on haematopoietic stem/progenitor cell (HSC) number and function and to examine the impact of modulating glycoprotein (GP)130 receptor in these cells.

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Angiotensin-Converting Enzyme 2: SARS-CoV-2 Receptor and Regulator of the Renin-Angiotensin System: Celebrating the 20th Anniversary of the Discovery of ACE2.

TL;DR: A review summarizes the progress over the past 20 years, highlighting the critical role of ACE2 as the novel SARS-CoV-2 receptor and as the negative regulator of the renin-angiotensin system, together with implications for the coronavirus disease 2019 pandemic and associated cardiovascular diseases.
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The Role of Inflammation in Diabetic Retinopathy

TL;DR: The relationship between early leukocytes activation and the later features of DR are discussed, common pathogenetic processes between diabetic microvascular disease and other vascular retinopathies, the mechanisms whereby leukocyte activation is induced in hyperglycemia and dyslipidemia, the signaling mechanisms involved in diabetic microVascular disease, and possible interventions which may prevent these retInopathies.
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Diabetes Mellitus and Ischemic Diseases Molecular Mechanisms of Vascular Repair Dysfunction

TL;DR: An overview of the current understanding on the signaling molecules contributing to the diabetes mellitus–induced impairment of postischemic revascularization mainly in the setting of myocardial infarction or critical limb ischemia is given.
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Sustained high glucose exposure sensitizes macrophage responses to cytokine stimuli but reduces their phagocytic activity

TL;DR: Long-term high glucose sensitizes macrophages to cytokine stimulation and reduces phagocytosis and nitric oxide production, which may be related to impaired glycolytic capacity.
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Microglia and Monocyte-Derived Macrophages in Stroke

TL;DR: A role for microglia and monocytes/macrophages in acute ischemic stroke in the context of normal and metabolically compromised conditions is summarized.
References
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Isolation of putative progenitor endothelial cells for angiogenesis.

TL;DR: It is suggested that EC progenitors may be useful for augmenting collateral vessel growth to ischemic tissues (therapeutic angiogenesis) and for delivering anti- or pro-angiogenic agents, respectively, to sites of pathologic or utilitarianAngiogenesis.
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The NOX Family of ROS-Generating NADPH Oxidases: Physiology and Pathophysiology

TL;DR: This review summarizes the current state of knowledge of the functions of NOX enzymes in physiology and pathology.
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Bone marrow cells regenerate infarcted myocardium

TL;DR: It is indicated that locally delivered bone marrow cells can generate de novo myocardium, ameliorating the outcome of coronary artery disease.
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Isolation and functional properties of murine hematopoietic stem cells that are replicating in vivo.

TL;DR: It is discovered that display of Hoechst fluorescence simultaneously at two emission wavelengths revealed a small and distinct subset of whole bone marrow cells that had phenotypic markers of multipotential HSC, which were shown in competitive repopulation experiments to contain the vast majority of HSC activity from murine bone marrow and to be enriched at least 1,000-fold for in vivo reconstitution activity.
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Bone-marrow adipocytes as negative regulators of the haematopoietic microenvironment

TL;DR: In lipoatrophic A-ZIP/F1 ‘fatless’ mice, and in mice treated with the peroxisome proliferator-activated receptor-γ inhibitor bisphenol A diglycidyl ether, marrow engraftment after irradiation is accelerated relative to wild-type or untreated mice, suggesting that antagonizing marrow adipogenesis may enhance haematopoietic recovery in clinical bone-marrow transplantation.
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