ArticleMolecular biology of the cell2025
Tetraspanin CD82 regulates transforming growth factor-β signaling in hematopoietic stem and progenitor cells.
Article in Molecular biology of the cell, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
1 citing paper in PubMed.
- Extracellular vesicle cargo dynamics in the bone marrow microenvironment: from hematopoietic homeostasis to malignant transformation.Extracellular vesicle · 2026Article
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Authors and funding
6 authors.
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Abstract
The cellular demand of the hematopoietic system is maintained by a rare pool of tissue-specific, hematopoietic stem cells (HSC). HSCs are primarily maintained in a quiescent state but can be activated to exit quiescence and undergo self-renewal and differentiation in response to stress. The cytokine transforming growth factor-β (TGF-β) plays an essential role in supporting HSC quiescence and activation, as one of the most potent inhibitors of hematopoietic stem and progenitor cell (HSPC) growth. Therefore, how TGF-β signaling can be regulated in the context of HSCs is of significant interest as it may uncover novel mechanisms to target HSC activity. Previous studies revealed that the tetraspanin CD82 modulates the long-term HSC population, with CD82 knockout (KO) mice displaying increased HSC activation. Here, in this study, we connect the CD82 scaffold with the regulation of TGF-β signaling in HSPCs. We show that CD82KO leads to decreased TGF-β signaling, whereas increased CD82 expression promotes TGF-β activation. These changes in CD82-mediated TGF-β signaling are associated with extracellular matrix interactions, as fibronectin engagement is critical for promoting TGF-β signaling. Mechanistically, we find that CD82 stimulates enhanced TGF-β activation by promoting receptor cross-talk between TGF-β receptor I and integrin β1, resulting in downstream changes in cell proliferation. Collectively, these findings demonstrate that CD82 modulates canonical TGF-β signaling through receptor cross-talk mechanisms that may be targeted to alter the balance between HSC quiescence and activation.
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