top of page
  • Zdjęcie autoraKrzysztof Szade

New paper for New Year! Our study in EMBO Reports shows HO-1 deficiency triggers exhaustion of HSCs

Zaktualizowano: 6 paź 2021

We are happy to share our new work on role of HO-1 on HSCs :)

We showed that HO-1 is highly expressed in the bone marrow niche, but its expression decreases during aging. Lack of HO-1 triggers premature aging of HSCs. We characterized the unique prematurely aged phenotype of HSC isolated from young HO-1-deficient mice on global transcriptome level. HSCs transplanted into HO‐1-deficient recipients exhaust their regenerative potential early and do not reconstitute secondary recipients. In turn, transplantation of HO‐1-deficient HSCs to the wild-type recipients recovers the regenerative potential of HO‐1-deficient HSCs and reverses their transcriptional alterations. Thus, HSC‐extrinsic activity of HO‐1 prevents HSCs from premature exhaustion and may restore the function of aged HSCs.


34 wyświetlenia0 komentarzy

Ostatnie posty

Zobacz wszystkie

留言


bottom of page