Peptides and other neuronal markers in transplanted pancreatic islets☆

Persson–Sjögren, Solveig; Forsgren, Sture; Täljedal, Inge‐Bert

doi:10.1016/s0196-9781(00)00186-8

Cited by 30 publications

(26 citation statements)

References 91 publications

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“…In fact, the presence of a local interaction between nociceptive fibres (which are responsive to insulin) and β-cells (which are responsive to neuropeptides such as SP) is thought to sustain islet homeostasis and glucose metabolism 126 . This is in agreement with data showing that sensory neurons are required for physiological β-cell function following transplants 127 . Interestingly, NOD mice have a hypofunctional version of TRPV1 that was shown to cause the disruption of this local regulatory feedback, thus influencing the early stages of islet inflammation 126 .…”

Section: Actions Of Neuropeptides On Immune Cellssupporting

confidence: 93%

Crosstalk between the nociceptive and immune systems in host defence and disease

2015

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Nociceptors and immune cells both protect the host from potential threats to homeostasis. There is growing evidence for bidirectional signalling between these two systems, and the underlying mechanisms are beginning to be elucidated. An understanding is emerging of how both the adaptive and innate immune systems can activate and sensitize nociceptors, and, reciprocally, how nociceptors modulate immune cells. In this Review, we discuss how these interactions can be adaptive and useful to the organism but also consider when such signalling might be maladaptive and pathophysiological, contributing to immune-mediated diseases and persistent pain states.

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Section: Actions Of Neuropeptides On Immune Cellssupporting

confidence: 93%

Crosstalk between the nociceptive and immune systems in host defence and disease

2015

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“…After implantation under the kidney capsule, the entire extrinsic innervation to the implanted islets is lost and is only slowly replaced by nerves growing in from surrounding structures, mainly in association with blood vessels [19,20]. Furthermore, neurones present in islet grafts do not seem to survive for more than up to 1 week after transplantation [21].…”

Section: Discussionmentioning

confidence: 99%

Neural crest stem cells increase beta cell proliferation and improve islet function in co-transplanted murine pancreatic islets

Olerud

Kanaykina²,

Vasilovska³

et al. 2009

Diabetologia

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“…For both clinical and experimental islet transplantation, approximately 60-80% of the transplanted islets are lost in the immediate posttransplant period (5,(13)(14)(15)(16). This rapid attrition of islet tissue is due, in part, to isolation-induced islet damage resulting from disruption of the islet vasculature and innervation (17,18) as well as detachment from the peri-islet basement membrane (BM) (19,20). To circumvent this problem, excessive numbers of islets are routinely transplanted in both experimental and clinical settings.…”

Section: Introductionmentioning

confidence: 99%

Islet Heparan Sulfate but Not Heparan Sulfate Proteoglycan Core Protein Is Lost During Islet Isolation and Undergoes Recovery Post-Islet Transplantation

Choong

Freeman

Parish

et al. 2015

American Journal of Transplantation

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Islet beta cells in situ express intracellular heparan sulfate (HS), a property previously shown in vitro to be important for their survival. We report that HS levels inside islet beta cells correlate with the novel intracel-lular localization of the HSPG core proteins for collagen type XVIII (Col18), a conventional extracellular matrix component. Syndecan-1 (Sdc1) and CD44 core proteins were similarly localized inside beta cells. During isolation, mouse islets selectively lose HS to 11-27% of normal levels but retain their HSPG core proteins. Intra-islet HS failed to recover substantially during culture for 4 days and was not reconstituted in vitro using HS mimetics. In contrast, significant recovery of intra-islet HS to $40-50% of normal levels occurred by 5-10 days after isotransplantation. Loss of islet HS during the isolation procedure is independent of heparanase (a HS-degrading endoglycosidase) and due, in part, to oxidative damage. Treatment with antioxidants reduced islet cell death by $60% and increased the HS content of isolated islets by $twofold compared to untreated islets, preserving intra-islet HS to $60% of the normal HS content of islets in situ. These findings suggest that the preservation of islet HS during the islet isolation process may optimize islet survival posttransplant. Abbreviations: AEC, 3-amino-9-ethylcarbazole; A.U., arbitrary units; B6.Hpse-KO, heparanase knockout C57BL/6; BHA, butylated hydroxyanisole; BM, basement membrane; Col18, collagen type XVIII; DMTU, dimethylthiourea; ECM, extracellular matrix; EXT1-2, exostosin 1-2; EXTL1-3, exostosin-like 1-3; FITC, fluo-rescein isothiocyanate; GMFR, geometric mean fluo-rescence ratio; Gpc2, glypican-2; H&E, haematoxylin and eosin; HS, heparan sulfate; HSPG, heparan sulfate proteoglycan; MFI, mean fluorescence intensity; MNCs, mononuclear cells; Ndst2, N-deacetylase/N-sulfotransferase 2; NOD/Lt, nonobese diabetic; PSN, penicillin-streptomycin-neomycin; qRT-PCR, quantitative reverse transcription polymerase chain reaction; ROS, reactive oxygen species; Sdc1, syndecan-1; SEM, standard error of the mean

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Peptides and other neuronal markers in transplanted pancreatic islets☆

Cited by 30 publications

References 91 publications

Crosstalk between the nociceptive and immune systems in host defence and disease

Crosstalk between the nociceptive and immune systems in host defence and disease

Neural crest stem cells increase beta cell proliferation and improve islet function in co-transplanted murine pancreatic islets

Islet Heparan Sulfate but Not Heparan Sulfate Proteoglycan Core Protein Is Lost During Islet Isolation and Undergoes Recovery Post-Islet Transplantation

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