ArticleInternational journal of stem cells2010
Notch and hedgehog signaling cooperate to maintain self-renewal of human embryonic stem cells exposed to low oxygen concentration.
Article in International journal of stem cells, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- The mouse allantois: new insights at the embryonic-extraembryonic interface.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2022Review
- Tgf-Beta family signaling in embryonic stem cells.International journal of stem cells · 2011Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
objectivesExpansion and maintenance of human embryonic stem cells (hESCs) in undifferentiated state is influenced by complex signals in the microenvironment, including those contingent upon oxygen availability. Responses mediated by Notch and Hedgehog (Hh) have essential role in the growth and maintenance of hESCs, therefore this study examined their effect on the self-renewal of hESCs exposed to low oxygen. METHODS AND
resultsUsing potent antagonists γ-secretase inhibitor and cyclopamine, we inhibited Notch and Hh pathways, respectively, in the CLS1 hESC line expanded continuously in a hypoxic atmosphere of 5% oxygen. Immunohistochemical staining and protein assays revealed loss of Oct4 and gain of stage-specific embryonic antigen 1 (SSEA1) markers in the inhibited cells. Semiquantitative real-time RT-PCR, and bromodeoxyuridine and thymidine incorporation assays demonstrated low Oct4 and Nanog mRNA expression, and decreased DNA synthesis, respectively, resulting from the block of each of the pathways. The loss increased significantly with co-inhibition of both pathways. Importantly, Notch and Hh downstream targets, including Hes1, Hey1, GIi1, and Ptc1, were surprisingly suppressed not only by the pathway-specific but also the unrelated inhibitor.
conclusionsThese findings demonstrate complementary effect of Notch and Hh signaling in hypoxia enhanced maintenance of hESCs.
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Registered trials
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