Reversal of Hyperglycemia by Insulin-Secreting Rat Bone Marrow- and Blastocyst-Derived Hypoblast Stem Cell-Like Cells
- Authors
- Kumar, Anujith; Lo Nigro, Antonio; Gysemans, Conny; Cai, Qing; Esguerra, Camila; Nelson-Holte, Molly; Heremans, Yves; Jimenez-Gonzalez, Maria; Porciuncula, Angelo; Mathieu, Chantal; Binas, Bert; Heimberg, Harry; Prosper, Felipe; Hering, Bernhard; Verfaillie, Catherine M.; Barajas, Miguel
- Issue Date
- May-2013
- Publisher
- Public Library of Science
- Keywords
- PROGENITOR CELLS; GENE; MOUSE PANCREAS; IN-VIVO; LIVER; PANCREATIC BETA-CELLS; ENDODERM; DIFFERENTIATION; EXPRESSION; CULTURE
- Citation
- PLoS ONE, v.8, no.5, pp 1 - 11
- Pages
- 11
- Indexed
- SCIE
SCOPUS
- Journal Title
- PLoS ONE
- Volume
- 8
- Number
- 5
- Start Page
- 1
- End Page
- 11
- URI
- https://scholarworks.bwise.kr/erica/handle/2021.sw.erica/28011
- DOI
- 10.1371/journal.pone.0063491
- ISSN
- 1932-6203
- Abstract
- beta-cell replacement may efficiently cure type 1 diabetic (T1D) patients whose insulin-secreting beta-cells have been selectively destroyed by autoantigen-reactive T cells. To generate insulin-secreting cells we used two cell sources: rat multipotent adult progenitor cells (rMAPC) and the highly similar rat extra-embryonic endoderm precursor (rXEN-P) cells isolated under rMAPC conditions from blastocysts (rHypoSC). rMAPC/rHypoSC were sequentially committed to definitive endoderm, pancreatic endoderm, and beta-cell like cells. On day 21, 20% of rMAPC/rHypoSC progeny expressed Pdx1 and C-peptide. rMAPCr/HypoSC progeny secreted C-peptide under the stimulus of insulin agonist carbachol, and was inhibited by the L-type voltage-dependent calcium channel blocker nifedipine. When rMAPC or rHypoSC differentiated d21 progeny were grafted under the kidney capsule of streptozotocin-induced diabetic nude mice, hyperglycemia reversed after 4 weeks in 6/10 rMAPC-and 5/10 rHypoSC-transplanted mice. Hyperglycemia recurred within 24 hours of graft removal and the histological analysis of the retrieved grafts revealed presence of Pdx1-, Nkx6.1- and C-peptide-positive cells. The ability of both rMAPC and HypoSC to differentiate to functional beta-cell like cells may serve to gain insight into signals that govern beta-cell differentiation and aid in developing culture systems to commit other (pluripotent) stem cells to clinically useful beta-cells for cell therapy of T1D.
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