Compare miRNA expression profiles of human iNSC, H9-NSC, fibroblast
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Kyung-Rok Yu
PROVIDER: E-GEOD-59301 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Advances in molecular strategies to reprogram cell fate is a promising avenue for cell-based therapies. Methods to generate induced neural stem cells (iNSCs) are often slow with limited reprogramming events and it is unclear whether cells transit via a pluripotent state. We report an iNSC reprogramming approach from embryonic and aged mouse fibroblasts using an engineered Sox17 (eSox17FNV). eSox17FNV efficiently drives iNSC reprogramming while Sox2 or Sox17 fails to do so. eSox17FNV acquires the capacity to bind new protein partners to scan the genome more efficiently and possesses a more potent transactivation domain than Sox2. At the onset of reprogramming, in the presence of eSox17FNV, fibroblasts divert from a iPSC route towards iNSC fate. Further, lineage tracing shows that emerging iNSCs do not transit through a pluripotent state if POU factors are excluded. This reveals new molecular and physiological framework for iNSC generation and contrasts with lineage from pluripotency reprogramming.
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Project description:Advances in molecular strategies to reprogram cell fate is a promising avenue for cell-based therapies. Methods to generate induced neural stem cells (iNSCs) are often slow with limited reprogramming events and it is unclear whether cells transit via a pluripotent state. We report an iNSC reprogramming approach from embryonic and aged mouse fibroblasts using an engineered Sox17 (eSox17FNV). eSox17FNV efficiently drives iNSC reprogramming while Sox2 or Sox17 fails to do so. eSox17FNV acquires the capacity to bind new protein partners to scan the genome more efficiently and possesses a more potent transactivation domain than Sox2. At the onset of reprogramming, in the presence of eSox17FNV, fibroblasts divert from a iPSC route towards iNSC fate. Further, lineage tracing shows that emerging iNSCs do not transit through a pluripotent state if POU factors are excluded. This reveals new molecular and physiological framework for iNSC generation and contrasts with lineage from pluripotency reprogramming.
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Project description:Advances in molecular strategies to reprogram cell fate is a promising avenue for cell-based therapies. Methods to generate induced neural stem cells (iNSCs) are often slow with limited reprogramming events and it is unclear whether cells transit via a pluripotent state. We report an iNSC reprogramming approach from embryonic and aged mouse fibroblasts using an engineered Sox17 (eSox17FNV). eSox17FNV efficiently drives iNSC reprogramming while Sox2 or Sox17 fails to do so. eSox17FNV acquires the capacity to bind new protein partners to scan the genome more efficiently and possesses a more potent transactivation domain than Sox2. At the onset of reprogramming, in the presence of eSox17FNV, fibroblasts divert from a iPSC route towards iNSC fate. Further, lineage tracing shows that emerging iNSCs do not transit through a pluripotent state if POU factors are excluded. This reveals new molecular and physiological framework for iNSC generation and contrasts with lineage from pluripotency reprogramming.
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Project description:Advances in molecular strategies to reprogram cell fate is a promising avenue for cell-based therapies. Methods to generate induced neural stem cells (iNSCs) are often slow with limited reprogramming events and it is unclear whether cells transit via a pluripotent state. We report an iNSC reprogramming approach from embryonic and aged mouse fibroblasts using an engineered Sox17 (eSox17FNV). eSox17FNV efficiently drives iNSC reprogramming while Sox2 or Sox17 fails to do so. eSox17FNV acquires the capacity to bind new protein partners to scan the genome more efficiently and possesses a more potent transactivation domain than Sox2. At the onset of reprogramming, in the presence of eSox17FNV, fibroblasts divert from a iPSC route towards iNSC fate. Further, lineage tracing shows that emerging iNSCs do not transit through a pluripotent state if POU factors are excluded. This reveals new molecular and physiological framework for iNSC generation and contrasts with lineage from pluripotency reprogramming.
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Project description:Brief expression of pluripotency-associated factors such as OCT4, KLF4, SOX2 and c-MYC (OKSM), in combination with differentiation-inducing signals, was reported to trigger transdifferentiation of fibroblasts into alternative cell types. Here, we show that OKSM expression gives rise to both induced pluripotent stem cells (iPSCs) and iNSCs under conditions that were previously shown to induce only NSC transdifferentiation. Fibroblast-derived iNSC colonies silenced retroviral transgenes and reactivated silenced X chromosomes, both hallmarks of pluripotent stem cells. Moreover, lineage tracing via an Oct4-CreER labeling system demonstrated that virtually all iNSC colonies originate from cells transiently expressing Oct4, whereas ablation of Oct4-positive cells prevented iNSC formation. Lastly, use of an alternative transdifferentiation cocktail that lacks OCT4 and was reportedly unable to support induced pluripotency, yielded iPSCs and iNSCs carrying the Oct4-CreER-derived lineage label. Together, these data suggest that iNSC generation using OKSM and related reprogramming factors requires passage through a transient iPSC state. 5 samples were anlyzed in total, 2 induced pluripotent stem cells (iPSCs), 1 neural stem cells (NSCs) and 2 induced NSCs (iNSCs)
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Project description:The iNSC cells are two clones generated from the same MEF line. Therefore, we conducted one analysis that compared the two clonal lines and a separate analysis that compared iNSC vs. NSC, iNSC vs. MEF, and NSC vs. MEF. Both were single factor ANOVAs, the first compared two groups (the iNSC lines) and the second had three groups. For the second analysis, we then used linear contrasts to extract the information about differences between all pairs (e.g. iNSC vs. NSC). Looking at the iNSC lines, the correlations between samples from different clonal lines are as high as the correlations between samples from within a clonal line. Given this, we think that the analysis that combines all 6 of them to compare against the other cell types is appropriate.
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