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Coculture of Insulin-Producing RIN5AH Cells With Neural Crest Stem Cells Protects Partially Against Cytokine-Induced Cell Death
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Neuroanatomy.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Neuroanatomy.
2012 (English)In: Pancreas, ISSN 0885-3177, E-ISSN 1536-4828, Vol. 41, no 3, 490-492 p.Article in journal, Letter (Refereed) Published
Place, publisher, year, edition, pages
2012. Vol. 41, no 3, 490-492 p.
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:uu:diva-173483DOI: 10.1097/MPA.0b013e31823fcf2aISI: 000301540300021OAI: oai:DiVA.org:uu-173483DiVA: diva2:523756
Available from: 2012-04-26 Created: 2012-04-25 Last updated: 2017-12-07Bibliographically approved
In thesis
1. The beneficial Effects of Neural Crest Stem Cells on Pancreatic      β–cells
Open this publication in new window or tab >>The beneficial Effects of Neural Crest Stem Cells on Pancreatic      β–cells
2014 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Patients with type-1 diabetes lose their β-cells after autoimmune attack. Islet transplantation is a co-option for curing this disease, but survival of transplanted islets is poor. Thus, methods to enhance β-cell viability and function as well as methods to expand β-cell mass are required. The work presented in this thesis aimed to study the roles of neural crest stem cells or their derivatives in supporting β-cell proliferation, function, and survival.

In co-culture when mouse boundary cap neural crest stem cells (bNCSCs) and pancreatic islets were in direct contact, differentiating bNCSCs strongly induced β-cell proliferation, and these proliferating β-cells were glucose responsive in terms of insulin secretion. Moreover, co-culture of murine bNCSCs with β-cell lines RIN5AH and β-TC6 showed partial protection of β-cells against cytokine-induced β-cell death. Direct contacts between bNCSCs and β-cells increased β-cell viability, and led to cadherin and β-catenin accumulations at the bNCSC/β-cell junctions. We proposed that cadherin junctions supported signals which promoted β-cell survival. We further revealed that murine neural crest stem cells harvested from hair follicles were unable to induce β-cell proliferation, and did not form cadherin junctions when cultured with pancreatic islets. Finally, we discovered that the presence of bNCSCs in co-culture counteracted cytokine-mediated insulin-producing human EndoC-βH1 cell death. Furthermore, these two cell types formed N-cadherin, but not E-cadherin, junctions when they were in direct contact. In conclusion, the results of these studies illustrate how neural crest stem cells influence β-cell proliferation, function, and survival which may improve islet transplantation outcome.

Place, publisher, year, edition, pages
Uppsala: Acta Universitatis Upsaliensis, 2014. 67 p.
Series
Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine, ISSN 1651-6206 ; 1037
Keyword
Neural Crest Stem Cells, Pancreatic Islets, β-cell proliferation, β-cell survival, Cadherin
National Category
Neurosciences
Research subject
Medical Science
Identifiers
urn:nbn:se:uu:diva-233157 (URN)978-91-554-9056-0 (ISBN)
Public defence
2014-11-18, B/B7:113a, Biomedical center, Husargatan 3, Uppsala, 13:15 (English)
Opponent
Supervisors
Available from: 2014-10-27 Created: 2014-09-29 Last updated: 2015-01-23

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Ngamjariyawat, AnongnadTurpaev, KyrilWelsh, NilsKozlova, Elena N.

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