Publication: Selective TGF-β1/ALK inhibitor improves neuronal differentiation of mouse embryonic stem cells
Issued Date
2014-08-22
Resource Type
ISSN
18727972
03043940
03043940
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2-s2.0-84903834706
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Mahidol University
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SCOPUS
Bibliographic Citation
Neuroscience Letters. Vol.578, (2014), 1-6
Suggested Citation
Nuttha Klincumhom, Theerawat Tharasanit, Chommanart Thongkittidilok, Narong Tiptanavattana, Sasitorn Rungarunlert, András Dinnyés, Mongkol Techakumphu Selective TGF-β1/ALK inhibitor improves neuronal differentiation of mouse embryonic stem cells. Neuroscience Letters. Vol.578, (2014), 1-6. doi:10.1016/j.neulet.2014.06.001 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/34887
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Title
Selective TGF-β1/ALK inhibitor improves neuronal differentiation of mouse embryonic stem cells
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Abstract
The transforming growth factor-β1 (TGF-β1), a polypeptide member of the TGF-β superfamily, has myriad cellular functions, including cell fate differentiation. We hypothesized that suppression of TGF-β1 signaling would improve the efficacy of neuronal differentiation during embryoid body (EB) development. In this study, mouse embryonic stem cells (ESCs) were allowed to differentiate into their neuronal lineage, both with, and without the TGF-β1 inhibitor (A83-01). After 8 days of EB suspension culture, the samples were examined by morphological analysis, immunocytochemistry and immunohistochemistry with pluripotent (Oct4, Sox2) and neuronal specific markers (Pax6, NeuN). The alteration of gene expressions during EB development was determined by quantitative RT-PCR. Our results revealed that the TGF-β1/ALK inhibitor potentially suppressed pluripotent gene (Oct4) during a rapidly up-regulation of neuronal associated genes including Sox1 and MAP2. Strikingly, during EB development, the expression of GFAP, the astrocyte specific gene, remarkably decreased compared to the non-treated control. This strategy demonstrated the beneficial function of TGF-β1/ALK inhibitor that rapidly and uniformly drives cell fate alteration from pluripotent state toward neuronal lineages. © 2014 Elsevier Ireland Ltd.