ArticleScience China. Life sciences2025
Dynamic WNT signaling controls differentiation of hematopoietic progenitor cells from human pluripotent stem cells.
Article in Science China. Life sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- The KXD1-TSPAN14 axis controls megakaryopoiesis and platelet production via Notch signaling.Science China. Life sciences · 2026Article
- Cyanine-modified ssODNs enhance CRISPR-Cas9 HDR in stem cell embryo models via chromatin and chemical modulation.Nature communications · 2026Article
- Wnt signaling dysregulation drives Stargardt disease pathogenesis.Science China. Life sciences · 2026Article
- Stable bioreactor control reveals acidic pH-driven metabolic reprogramming and mitochondrial dysfunction in human lymphoblastoid cells.Communications biology · 2026Article
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Authors and funding
19 authors.
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Abstract
Human pluripotent stem cells (hPSCs) can in theory give rise to any hematopoietic lineages, thereby offering opportunities for disease modeling, drug screening and cell therapies. However, gaps in our knowledge of the signaling requirements for the specification of human hematopoietic stem/progenitor cells (HSPCs), which lie at the apex of all hematopoietic lineages, greatly limit the potential of hPSC in hematological research and application. Transcriptomic analysis reveals aberrant regulation of WNT signaling during maturation of hPSC-derived hematopoietic progenitor cells (hPSC-HPCs), which results in higher mitochondria activity, misregulation of HOX genes, loss of self-renewal and precocious differentiation. These defects are partly due to the activation of the WNT target gene CDX2. Late-stage WNT inhibition improves the yield, self-renewal, multilineage differentiation, and transcriptional and metabolic profiles of hPSC-HPCs. Genome-wide mapping of transcription factor (TF) accessible chromatin reveals a significant overrepresentation of myeloid TF binding motifs in hPSC-HPCs, which could underlie their myeloid-biased lineage potential. Together our findings uncover a previously unappreciated dynamic requirement of the WNT signaling pathway during the specification of human HSPCs. Modulating the WNT pathway with small molecules normalizes the molecular differences between hPSC-HPCs and endogenous hematopoietic stem cells (HSCs), thereby representing a promising approach to improve the differentiation and function of hPSC-HPCs.
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