Authors
Vanessa N Montinelli, Samantha Grohe, Xue Ying Song, Jacqueline Judith Turnlund, Hannah Hackbart, Joshua P Sasine, Morgan Brady, Masahiro Muraoka, Rucha Kadam, Flavia Cavicchioli, Sage Victoria Kang, Ashley Dawson, Mimoli Ellise Uehara, Courtny Dizon, Kurt Hankenson, Theresa Krack, Peibin Yue, Yuwei He, John P Chute
Published in
Blood. Jul 01, 2026. Epub Jul 01, 2026.
Abstract
Hematopoietic stem cells (HSCs) depend upon paracrine signals from bone marrow endothelial cells (BM ECs) and perivascular stromal cells for their maintenance and regeneration. Chemotherapy and total body irradiation (TBI) utilized in the curative treatment of cancer cause profound damage to the BM vascular niche, which impedes hematopoietic reconstitution. The mechanisms controlling regeneration of the HSC vascular niche are not well understood. We discovered that conditional deletion of R spondin 2 (Rspo2) from BM endothelial cells (ECs) impaired HSC regeneration in mice following total body irradiation (TBI), in association with decreased HSC survival. Mice lacking EC - Rspo2 expression demonstrated delayed regeneration of the BM vascular niche following TBI and Rspo2 - deficient BM ECs displayed defective angiogenesis. Conversely, systemic administration of R spondin 2 caused early restoration of the BM sinusoidal vascular niche in irradiated mice and augmented BM EC angiogenesis. Concordantly, R spondin 2 - treated mice displayed accelerated regeneration of the HSC pool. These studies suggest that BM ECs regulate the regeneration of the BM sinusoidal vascular niche via secretion of R spondin 2.
PMID:
42462108
Bibliographic data and abstract were imported from PubMed on 17 Jul 2026.
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