P.120: Additive Manufactured Macroencapsulation Devices for Islet Cell Replacement Therapy

Loss of photoreceptors due to retinal degeneration is a major cause of untreatable visual impairment and blindness. Cell replacement therapy, using retinal stem cell (RSC)-derived photoreceptors, holds promise for reconstituting...

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Adult Neural Progenitor Cells and Cell Replacement Therapy for Huntington Disease

Stem Cells & Regenerative Medicine - Stem Cell Biology and Regenerative Medicine ◽

10.1007/978-1-60761-860-7_18 ◽

2010 ◽

pp. 299-314 ◽

Cited By ~ 1

Author(s):

Bronwen Connor

Keyword(s):

Replacement Therapy ◽

Progenitor Cells ◽

Huntington Disease ◽

Neural Progenitor Cells ◽

Neural Progenitor ◽

Cell Replacement Therapy ◽

Cell Replacement

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ENTPD3 Marks Mature Stem Cell Derived Beta Cells Formed by Self-Aggregation in Vitro

10.2337/figshare.15124980.v1 ◽

2021 ◽

Author(s):

Fiona M. Docherty ◽

Kent A. Riemondy ◽

Roberto Castro-Gutierrez ◽

JaeAnn M. Dwulet ◽

Ali H. Shilleh ◽

...

Keyword(s):

Stem Cell ◽

Replacement Therapy ◽

Beta Cells ◽

Nucleoside Triphosphate ◽

Specific Marker ◽

Detailed Knowledge ◽

Cell Replacement Therapy ◽

Mature Adult ◽

Cell Replacement

Stem cell derived beta-like cells (sBC) carry the promise of providing an abundant source of insulin-producing cells for use in cell replacement therapy for patients with diabetes, potentially allowing widespread implementation of a practical cure. To achieve their clinical promise, sBC need to function comparably to mature adult beta cells, but as yet they display varying degrees of maturity. Indeed, detailed knowledge of the events resulting in human beta cell maturation remains obscure. Here we show that sBC spontaneously self-enrich into discreet islet-like cap structures within <i>in vitro</i> cultures, independent of exogenous maturation conditions. Multiple complementary assays demonstrate that this process is accompanied by functional maturation of the self-enriched sBC (seBC); however, the seBC still contain distinct subpopulations displaying different maturation levels. Interestingly, the surface protein ENTPD3 (also known as nucleoside triphosphate diphosphohydrolase-3 (NDPTase3)) is a specific marker of the most mature seBC population and can be used for mature seBC identification and sorting. Our results illuminate critical aspects of <i>in vitro</i> sBC maturation and provide important insights towards developing functionally mature sBC for diabetes cell replacement therapy.

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Ca(2+) Oscillations and Its Transporters in Mesenchymal Stem Cells

Physiological Research ◽

10.33549/physiolres.931734 ◽

2010 ◽

pp. 323-329 ◽

Cited By ~ 1

Author(s):

B Ye

Keyword(s):

Tissue Engineering ◽

Stem Cells ◽

Mesenchymal Stem Cells ◽

Replacement Therapy ◽

Cell Types ◽

Cell Replacement Therapy ◽

Cell Replacement ◽

Cell Functions ◽

The Past ◽

Intracellular Ca

Intracellular free Ca(2+) is one of important biological signals regulating a number of cell functions. It has been discussed widely and extensively in several cell types during the past two decades. Attention has been paid to the Ca2+ transportation in mesenchymal stem cells in recent years as mesenchymal stem cells have gained considerable interest due to their potential for cell replacement therapy and tissue engineering. In this paper, roles of intracellular Ca(2+) oscillations and its transporters in mesenchymal stem cells have been reviewed.

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Cell Replacement Therapy in Acute Stroke: Current State

Stem Cell and Gene-Based Therapy ◽

10.1007/1-84628-142-3_8 ◽

2006 ◽

pp. 123-132 ◽

Cited By ~ 1

Author(s):

Yossi Gilgun-Sherki ◽

Jonathan Y. Streifler

Keyword(s):

Acute Stroke ◽

Replacement Therapy ◽

Cell Replacement Therapy ◽

Cell Replacement ◽

Current State

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Transplanted Oligodendrocyte Progenitor Cells Survive in the Brain of a Rat Neonatal White Matter Injury Model but Less Mature in Comparison with the Normal Brain

Cell Transplantation ◽

10.1177/0963689720946092 ◽

2020 ◽

Vol 29 ◽

pp. 096368972094609

Author(s):

Shino Ogawa ◽

Mutsumi Hagiwara ◽

Sachiyo Misumi ◽

Naoki Tajiri ◽

Takeshi Shimizu ◽

...

Keyword(s):

White Matter ◽

Replacement Therapy ◽

Fluorescent Protein ◽

White Matter Injury ◽

Normal Brain ◽

Cell Replacement Therapy ◽

Cell Replacement ◽

Vitro Effect ◽

The Brain

Preterm infants have a high risk of neonatal white matter injury (WMI) caused by hypoxia-ischemia. Cell-based therapies are promising strategies for neonatal WMI by providing trophic substances and replacing lost cells. Using a rat model of neonatal WMI in which oligodendrocyte progenitors (OPCs) are predominantly damaged, we investigated whether insulin-like growth factor 2 (IGF2) has trophic effects on OPCs in vitro and whether OPC transplantation has potential as a cell replacement therapy. Enhanced expression of Igf2 mRNA was first confirmed in the brain of P5 model rats by real-time polymerase chain reaction. Immunostaining for IGF2 and its receptor IGF2 R revealed that both proteins were co-expressed in OLIG2-positive and GFAP-positive cells in the corpus callosum (CC), indicating autocrine and paracrine effects of IGF2. To investigate the in vitro effect of IGF2 on OPCs, IGF2 (100 ng/ml) was added to the differentiation medium containing ciliary neurotrophic factor (10 ng/ml) and triiodothyronine (20 ng/ml), and IGF2 promoted the differentiation of OPCs into mature oligodendrocytes. We next transplanted rat-derived OPCs that express green fluorescent protein into the CC of neonatal WMI model rats without immunosuppression and investigated the survival of grafted cells for 8 weeks. Although many OPCs survived for at least 8 weeks, the number of mature oligodendrocytes was unexpectedly small in the CC of the model compared with that in the sham-operated control. These findings suggest that the mechanism in the brain that inhibits differentiation should be solved in cell replacement therapy for neonatal WMI as same as trophic support from IGF2.

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The hematopoietic stem cells of alpha-thalassemic mice

Blood ◽

10.1182/blood.v66.3.595.595 ◽

1985 ◽

Vol 66 (3) ◽

pp. 595-601 ◽

Cited By ~ 5

Author(s):

JE Barker ◽

E McFarland

Keyword(s):

Stem Cells ◽

Replacement Therapy ◽

Host Cells ◽

Stem Cell Population ◽

Normal Donor ◽

Potential Candidate ◽

Cell Replacement Therapy ◽

Hematopoietic Stem ◽

Cell Replacement ◽

Marrow Cells

Abstract The alpha-thalassemic mouse has a hereditary microcytic anemia, almost certainly has a shortened RBC life span, and is a potential candidate for cell replacement therapy. In a routine study of bone marrow repopulating capacity using hemoglobin as a cell marker, normal donor marrow cells, but not alpha-thalassemic donor marrow cells, completely replaced the host cells. Further analysis showed that at least 30 times more alpha-thalassemic cells were required to outcompete normal donor cells injected simultaneously. The results were more extreme then expected and suggested a defect in a stem cell population as well as in the RBCs. Evidence that the multipotent and erythroid-committed stem cells in alpha-thalassemic mice are not decreased was shown by CFU-S and CFU-E assays. The combined results indicate that the deletion expresses itself most conspicuously in the RBC population. Tests were also performed to analyze repopulation kinetics in the Hbath-J/+ mice. In unirradiated alpha-thalassemic hosts, the hemoglobin from a normal donor persisted but did not replace the host hemoglobin. Sublethally irradiated alpha-thalassemic hosts, on the other hand, were easily repopulated with normal cells. We conclude that the alpha-thalassemic mouse is a good model for cell replacement therapy.

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