Defining the nature of human pluripotent stem cell progeny
Open accessAbstract
While it is clear that human pluripotent stem cells (hPSCs) can differentiate to generate a panoply of various cell types, it is unknown how closely in vitro development mirrors that which occurs in vivo. To determine whether human embryonic stem cells (hESCs) and human-induced pluripotent stem cells (hiPSCs) make equivalent progeny, and whether either makes cells that are analogous to tissue-derived cells, we performed comprehensive transcriptome profiling of purified PSC derivatives and their tissue-derived counterparts. Expression profiling demonstrated that hESCs and hiPSCs make nearly identical progeny for the neural, hepatic, and mesenchymal lineages, and an absence of re-expression from exogenous reprogramming factors in hiPSC progeny. However, when compared to a tissue-derived counterpart, the progeny of both hESCs and hiPSCs maintained expression of a subset of genes normally associated with early mammalian development, regardless of the type of cell generated. While pluripotent genes (OCT4, SOX2, REX1, and NANOG) appeared to be silenced immediately upon differentiation from hPSCs, genes normally unique to early embryos (LIN28A, LIN28B, DPPA4, and others) were not fully silenced in hPSC derivatives. These data and evidence from expression patterns in early human fetal tissue (3-16 weeks of development) suggest that the differentiated progeny of hPSCs are reflective of very early human development (< 6 weeks). These findings provide support for the idea that hPSCs can serve as useful in vitro models of early human development, but also raise important issues for disease modeling and the clinical application of hPSC derivatives.
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iPSC neurons exhibit a fetal neuronal identity that might not be optimally suited to model all disease-relevant phenotypes.
“They are also known to exhibit a fetal neuronal identity that might not be optimally suited to model all disease-relevant phenotypes (Arbab et al., 2014; Luo et al., 2016; Patterson et al., 2012).”
From Age-dependent instability of mature neuronal fate in induced neurons from Alzheimer’s patients (2021) · cites this paper as Patterson et al., 2012
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- Authors
- Patterson, M., Chan, D. N., Ha, I., Case, D., Cui, Y., Handel, B. V., Mikkola, H. K., & Lowry, W. E.
- Affiliations
- University of California, Los Angeles (US)
- Corresponding author
- Lowry, William E
- Venue
- Cell Research
- Published
- 2011-08-16
- Volume
- 22
- Issue
- 1
- Pages
- 178-193
- ISSN
- 1001-0602 (ISSN-L)
- 1748-7838
- PMC
- PMC3351932
- OpenAlex
- W2077007919
- Cited by
- 145
- References
- 52
- Citations by year
- 2026: 4 · 2025: 6 · 2024: 3 · 2023: 6 · 2022: 9 · 2021: 11 · 2020: 5 · 2019: 6 · 2018: 11 · 2017: 11 · 2016: 10 · 2015: 12 · 2014: 13 · 2013: 22 · 2012: 12
- FWCI
- 6.58
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Cell Research (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of General Medical Sciences (T32GM007104, GM007104-33)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Pluripotent Stem Cells Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Keywords
- human pluripotent stem cells, human embryonic stem cells, human induced pluripotent stem cells, in vitro differentiation, gene expression profiling, early human development, neural lineage, mesenchymal lineage, pluripotency genes, LIN28A, DPPA4, disease modeling
- MeSH terms
- Cell Differentiation, Embryo, Mammalian, Fibroblasts, Germ Layers, Humans, Transfection, Cluster Analysis, RNA-Binding Proteins, Gene Expression Regulation, Developmental, Cell Lineage, Gene Silencing, Gene Expression Profiling, Hepatocytes, Pluripotent Stem Cells, Embryonic Development, Octamer Transcription Factor-3, SOXB1 Transcription Factors, Neural Stem Cells, Cellular Reprogramming
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