Elevated Hedgehog activity contributes to attenuated DNA damage responses in aged hematopoietic cells.


Journal

Leukemia
ISSN: 1476-5551
Titre abrégé: Leukemia
Pays: England
ID NLM: 8704895

Informations de publication

Date de publication:
04 2020
Historique:
received: 08 05 2019
accepted: 03 11 2019
revised: 04 10 2019
pubmed: 16 11 2019
medline: 2 9 2020
entrez: 16 11 2019
Statut: ppublish

Résumé

Accumulation of DNA damage and myeloid-skewed differentiation characterize aging of the hematopoietic system, yet underlying mechanisms remain incompletely understood. Here, we show that aging hematopoietic progenitor cells particularly of the myeloid branch exhibit enhanced resistance to bulky DNA lesions-a relevant type of DNA damage induced by toxins such as cancer drugs or endogenous aldehydes. We identified aging-associated activation of the Hedgehog (Hh) pathway to be connected to this phenotype. Inhibition of Hh signaling reverts DNA damage tolerance and DNA damage-resistant proliferation in aged hematopoietic progenitors. Vice versa, elevating Hh activity in young hematopoietic progenitors is sufficient to impair DNA damage responses. Altogether, these findings provide experimental evidence for aging-associated increases in Hh activity driving DNA damage tolerance in myeloid progenitors and myeloid-skewed differentiation. Modulation of Hh activity could thus be explored as a therapeutic strategy to prevent DNA damage tolerance, myeloid skewing, and disease development in the aging hematopoietic system.

Identifiants

pubmed: 31728056
doi: 10.1038/s41375-019-0641-3
pii: 10.1038/s41375-019-0641-3
pmc: PMC7214262
doi:

Substances chimiques

Hedgehog Proteins 0
Veratrum Alkaloids 0
cyclopamine ZH658AJ192

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1125-1134

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Auteurs

Annika Scheffold (A)

Department of Internal Medicine III, University Hospital Ulm, 89081, Ulm, Germany.

Ali H Baig (AH)

Leibniz Institute on Aging, Fritz Lipmann Institute, 07745, Jena, Germany.

Zhiyang Chen (Z)

Leibniz Institute on Aging, Fritz Lipmann Institute, 07745, Jena, Germany.

Sarah E von Löhneysen (SE)

Leibniz Institute on Aging, Fritz Lipmann Institute, 07745, Jena, Germany.

Friedrich Becker (F)

Leibniz Institute on Aging, Fritz Lipmann Institute, 07745, Jena, Germany.

Yohei Morita (Y)

Leibniz Institute on Aging, Fritz Lipmann Institute, 07745, Jena, Germany.

Alush I Avila (AI)

Leibniz Institute on Aging, Fritz Lipmann Institute, 07745, Jena, Germany.

Marco Groth (M)

Leibniz Institute on Aging, Fritz Lipmann Institute, 07745, Jena, Germany.

André Lechel (A)

Department of Internal Medicine I, University Hospital Ulm, 89081, Ulm, Germany.

Florian Schmid (F)

Institute of Medical Systems Biology, Ulm University, 89081, Ulm, Germany.

Johann M Kraus (JM)

Institute of Medical Systems Biology, Ulm University, 89081, Ulm, Germany.

Hans A Kestler (HA)

Institute of Medical Systems Biology, Ulm University, 89081, Ulm, Germany.

Stephan Stilgenbauer (S)

Department of Internal Medicine III, University Hospital Ulm, 89081, Ulm, Germany.

Melanie Philipp (M)

Institute of Biochemistry and Molecular Biology, Ulm University, 89081, Ulm, Germany.
Department of Experimental and Clinical Pharmacology and Pharmacogenomics, Division of Pharmacogenomics, University of Tübingen, 72074, Tübingen, Germany.

Martin D Burkhalter (MD)

Institute of Biochemistry and Molecular Biology, Ulm University, 89081, Ulm, Germany. martin.burkhalter@uni-tuebingen.de.
Department of Experimental and Clinical Pharmacology and Pharmacogenomics, Division of Pharmacogenomics, University of Tübingen, 72074, Tübingen, Germany. martin.burkhalter@uni-tuebingen.de.

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