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.
