ArticleExperimental hematology2025
KLF4 enhances transplantation-induced hematopoiesis by inhibiting TLRs and noncanonical NFκB signaling at a steady state.
Article in Experimental hematology, 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.
- An inflammatory and quiescent HSC subpopulation expands with age in humans.Genome biology · 2026Article
- RAGER: A user-friendly computational platform for integrated analysis of RNA-Seq and ATAC-seq data.PloS one · 2026Article
- An Inflammatory and Quiescent HSC Subpopulation Expands with Age in Humans.bioRxiv : the preprint server for biology · 2025Article
- The reprogramming factor KLF4 in normal and malignant blood cells.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
The transcription factor Krüppel-like factor 4 (KLF4) acts as a transcriptional activator and repressor. KLF4 plays a role in various cellular processes, including the dedifferentiation of somatic cells into induced pluripotent stem cells. Although it has been shown to enhance self-renewal in embryonic and leukemia stem cells, its role in adult hematopoietic stem cells (HSCs) remains underexplored. We demonstrate that conditional deletion of the Klf4 gene in hematopoietic cells led to an increased frequency of immunophenotypic HSCs in the bone marrow, along with a normal distribution of lymphoid and myeloid progenitor cells. Noncompetitive bone marrow transplants showed normal engraftment and multilineage reconstitution, except for monocytes and T cells. However, the loss of KLF4 hindered hematologic reconstitution in competitive serial bone marrow transplants, highlighting a critical role for KLF4 in stress-induced hematopoiesis. Transcriptome analysis revealed an upregulation of NFκB2 and toll-like receptors (e.g., TLR4) in Klf4-null HSCs during homeostasis. Flow cytometry and immunoblot analysis confirmed the increased cell surface expression of TLR4 and the activation of NFκB2 in HSCs under homeostatic conditions, whereas NFκB2 expression drops after radiation compared with steady-state levels. Our findings suggest that the constitutive activation of the TLR4-NFκB2 pathway inhibits the ability of HSCs to regenerate blood after transplantation in cytoablated bone marrow.
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