The pancreatic islet endothelial cell: Emerging roles in islet function and disease

Olsson, Richard F.; Carlsson, Per‐Ola

doi:10.1016/j.biocel.2005.06.021

Cited by 53 publications

(30 citation statements)

References 17 publications

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“…The CD86 costimulatory factor can bind to either CD28 presented on the T cell (for autoregulation and intercellular association) and to CTLA4 synthesized by the T cell (to attenuate immune suppression and cellular disassociation). Pancreatic islet endothelial cells (ECs) were shown to form a barrier to autoreactive T cell transmigration during the development of islet inflammation in the development of IDDM (53, 54). In a study conducted by Lozanoska-Ochser et al, the goal was to determine the significance of costimulatory molecule synthesis by islet ECs.…”

Section: The Impact Of DC Costimulation On the Induction Of Iddmmentioning

confidence: 99%

The Role of Dendritic Cell Maturation in the Induction of Insulin-Dependent Diabetes Mellitus

et al. 2017

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Dendritic cells (DCs) are the dominant class of antigen-presenting cells in humans and are largely responsible for the initiation and guidance of innate and adaptive immune responses involved in maintenance of immunological homeostasis. Immature dendritic cells (iDCs) phagocytize pathogens and toxic proteins and in endosomal vesicles degrade them into small fragments for presentation on major histocompatibility complex (MHC) II receptor molecules to naïve cognate T cells (Th0). In addition to their role in stimulation of immunity, DCs are involved in the induction and maintenance of immune tolerance toward self-antigens. During activation, the iDCs become mature. Maturation begins when the DCs cease taking up antigens and begin to migrate from their location in peripheral tissues to adjacent lymph nodes or the spleen where during their continued maturation the DCs present stored antigens on surface MHCII receptor molecules to naive Th0 cells. During antigen presentation, the DCs upregulate the biosynthesis of costimulatory receptor molecules CD86, CD80, CD83, and CD40 on their plasma membrane. These activated DC receptor molecules bind cognate CD28 receptors presented on the Th0 cell membrane, which triggers DC secretion of IL-12 or IL-10 cytokines resulting in T cell differentiation into pro- or anti-inflammatory T cell subsets. Although basic concepts involved in the process of iDC activation and guidance of Th0 cell differentiation have been previously documented, they are poorly defined. In this review, we detail what is known about the process of DC maturation and its role in the induction of insulin-dependent diabetes mellitus autoimmunity.

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Section: The Impact Of DC Costimulation On the Induction Of Iddmmentioning

confidence: 99%

The Role of Dendritic Cell Maturation in the Induction of Insulin-Dependent Diabetes Mellitus

et al. 2017

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“…2; data reviewed in detail below). The concept of a signalling loop operating between the islet microvasculature and beta cell is well established in rodents and has been reviewed elsewhere [2–4]. Many studies have focused on the importance of the islet endothelial cell during beta cell development or in driving the programing of pluripotent stem cells toward a beta cell lineage, and revascularisation of islets following transplantation.…”

Section: Islet Vasculature: Not Just a Pretty Tubementioning

confidence: 99%

“…Based, in part, upon [2, 4]. Islet endothelial cells produce factors that enhance beta cell proliferation, survival and function under physiological conditions, including HGF, fibroblast growth factor (FGF), CTGF and THBS1.…”

Section: Figmentioning

confidence: 99%

The islet endothelial cell: a novel contributor to beta cell secretory dysfunction in diabetes

Hogan

Hull

2017

Diabetologia

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The pancreatic islet is highly vascularised, with an extensive capillary network. In addition to providing nutrients and oxygen to islet endocrine cells and transporting hormones to the peripheral circulation, islet capillaries (comprised primarily of islet endothelial cells) are an important source of signals that enhance survival and function of the islet beta cell. In type 2 diabetes, and animal models thereof, evidence exists of morphological and functional abnormalities in these islet endothelial cells. In diabetes, islet capillaries are thickened, dilated and fragmented, and islet endothelial cells express markers of inflammation and activation. In vitro data suggests that this dysfunctional islet endothelial phenotype may contribute to impaired insulin release from the beta cell. This review examines potential candidate molecules that may mediate the positive effects of islet endothelial cells on beta cell survival and function under normal conditions. Further, it explores possible mechanisms underlying the development of islet endothelial dysfunction in diabetes and reviews therapeutic options for ameliorating this aspect of the islet lesion in type 2 diabetes. Finally, considerations regarding differences between human and rodent islet vasculature and the potentially unforeseen negative consequences of strategies to expand the islet vasculature, particularly under diabetic conditions, are discussed.

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“…These include the well-recognized endocrine α, β, δ, and pancreatic polypeptide (PP) cell types, producing predominantly the hormones glucagon, insulin, somatostatin, and pancreatic polypeptide, respectively (Baetens et al 1979; Halban 2004). The extensive intra-islet capillary network comprises endothelial cells, together with supporting pericytes and fibroblasts (Ballian and Brunicardi 2007; Olsson and Carlsson 2006). Sympathetic and parasympathetic fibers innervate the islet (Ahren 2000) and also require supporting cells such as Schwann cells (Smith 1975).…”

mentioning

confidence: 99%

Hyaluronan and Hyaluronan Binding Proteins Are Normal Components of Mouse Pancreatic Islets and Are Differentially Expressed by Islet Endocrine Cell Types

Hull

Johnson

Braun

et al. 2012

J Histochem Cytochem.

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The pancreatic islet comprises endocrine, vascular, and neuronal cells. Signaling among these cell types is critical for islet function. The extracellular matrix (ECM) is a key regulator of cell-cell signals, and while some islet ECM components have been identified, much remains unknown regarding its composition. We investigated whether hyaluronan, a common ECM component that may mediate inflammatory events, and molecules that bind hyaluronan such as versican, tumor necrosis factor–stimulated gene 6 (TSG-6), and components of inter-α-trypsin inhibitor (IαI), heavy chains 1 and 2 (ITIH1/ITIH2), and bikunin, are normally produced in the pancreatic islet. Mouse pancreata and isolated islets were obtained for microscopy (with both paraformaldehyde and Carnoy’s fixation) and mRNA. Hyaluronan was present predominantly in the peri-islet ECM, and hyaluronan synthase isoforms 1 and 3 were also expressed in islets. Versican was produced in α cells; TSG-6 in α and β cells; bikunin in α, β, and δ cells; and ITIH1/ITIH2 predominantly in β cells. Our findings demonstrate that hyaluronan, versican, TSG-6, and IαI are normal islet components and that different islet endocrine cell types contribute these ECM components. Thus, dysfunction of either α or β cells likely alters islet ECM composition and could thereby further disrupt islet function.

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The pancreatic islet endothelial cell: Emerging roles in islet function and disease

Cited by 53 publications

References 17 publications

The Role of Dendritic Cell Maturation in the Induction of Insulin-Dependent Diabetes Mellitus

The Role of Dendritic Cell Maturation in the Induction of Insulin-Dependent Diabetes Mellitus

The islet endothelial cell: a novel contributor to beta cell secretory dysfunction in diabetes

Hyaluronan and Hyaluronan Binding Proteins Are Normal Components of Mouse Pancreatic Islets and Are Differentially Expressed by Islet Endocrine Cell Types

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