Tumor formation in cell replacement therapy using human ES cells

2009 ◽  
Vol 65 ◽  
pp. S9
Author(s):  
Jun Takahashi ◽  
Daisuke Doi ◽  
Asuka Morizane
Keyword(s):  
Replacement Therapy ◽  
Es Cells ◽  
Tumor Formation ◽  
Cell Replacement Therapy ◽  
Cell Replacement ◽  
Human Es Cells

An in vitro mouse model for retinal ganglion cell replacement therapy using eye-like structures differentiated from ES cells

2007 ◽  
Vol 84 (5) ◽  
pp. 868-875 ◽  
Author(s):  
Hitomi Aoki ◽  
Akira Hara ◽  
Masayuki Niwa ◽  
Tsutomu Motohashi ◽  
Takashi Suzuki ◽  
...  
Keyword(s):  
Mouse Model ◽  
Ganglion Cell ◽  
Replacement Therapy ◽  
Retinal Ganglion Cell ◽  
Es Cells ◽  
Retinal Ganglion ◽  
Cell Replacement Therapy ◽  
Cell Replacement

scholarly journals In Vivo Differentiation of Mouse Embryonic Stem Cells into Hepatocytes

2002 ◽  
Vol 11 (4) ◽  
pp. 359-368 ◽  
Author(s):  
Dongho Choi ◽  
Hyun-Jeong Oh ◽  
Uck-Jin Chang ◽  
Soo Kyung Koo ◽  
Jean X. Jiang ◽  
...  
Keyword(s):  
Replacement Therapy ◽  
Es Cells ◽  
Embryonic Stem ◽  
Cell Replacement Therapy ◽  
Differentiation Potential ◽  
Cell Replacement ◽  
Mouse Es Cells ◽  
Cord Injury ◽  
In Vivo Differentiation

Embryonic stem (ES) cells have been regarded as a powerful resource for cell replacement therapy. In recent reports mouse ES cells have been successfully applied in the treatment of spinal cord injury, hereditary myelin disorder of the central nervous system, and diabetes mellitus. Another type of disease that could benefit from the availability of stem cell therapy is liver disease. However, for this potential to be realized, it is necessary to demonstrate the differentiation of ES cells into hepatocytes. To demonstrate the in vivo differentiation potential of mouse ES cells, we injected ES cells into the spleen of immunosuppressed nude mice. Histological analysis of teratomas derived from injected ES cells revealed that some areas contained typical hepatocytes arranged in a sinusoidal structure. The hepatic nature of these cells was further confirmed by showing that transcripts of liver-specific genes were present in the differentiated teratoma using reverse transcriptase-polymerase chain reaction and immunohistochemistry using several liver-specific antibodies including HEP-PAR, phenylalanine hydroxylase, and mouse N-system aminotransferase to identify the respective proteins in the differentiated hepatocytes. This is the first demonstration that mouse ES cells can differentiate in vivo into a mixed population of hepatocytes of varying maturity. This finding extends the potential use of ES cells in the cell replacement therapy by including its possible application for treating liver diseases.

A microfluidic platform enables comprehensive gene expression profiling of mouse retinal stem cells

Lab on a Chip ◽  
2021 ◽  
Author(s):  
Shana O Kelley ◽  
Mahmoud Labib ◽  
Brenda Coles ◽  
Mahla Poudineh ◽  
Brendan Innes ◽  
...  
Keyword(s):  
Gene Expression ◽  
Stem Cells ◽  
Stem Cell ◽  
Visual Impairment ◽  
Gene Expression Profiling ◽  
Replacement Therapy ◽  
Retinal Degeneration ◽  
Expression Profiling ◽  
Cell Replacement Therapy ◽  
Cell Replacement

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...

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

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.

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

2010 ◽  
pp. 323-329 ◽  
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.

scholarly journals 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

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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