Tif1γ regulates the TGF-β1 receptor and promotes physiological aging of hematopoietic stem cells

Quéré, Ronan; Saint-Paul, Laetitia; Carmignac, Virginie; Martin, Romain Z.; Chrétien, Marie‐Lorraine; Largeot, Anne; Hammann, Arlette; Barros, Jean‐Paul Pais de; Bastie, Jean-Noël; Delva, Laurent

doi:10.1073/pnas.1405546111

Cited by 62 publications

(45 citation statements)

References 45 publications

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“…TGFβ1 appeared to have differential regulatory effects on different subsets of HSCs, stimulating myeloid-biased HSCs to proliferate while inhibiting lymphoid-biased HSCs [49]. Mechanistically, TGFβ1 signaling in HSCs was regulated in part by transcription intermediary factor 1γ (Tif1γ) and RNA binding protein Musashi 2 (Msi-2) [50, 51]. …”

Section: Regulation Of Stress-induced Hematopoiesis By Cytokine Signamentioning

confidence: 99%

Regulation of stress-induced hematopoiesis

Zhao

Baltimore²

2015

Current Opinion in Hematology

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Purpose of review Hematopoietic stem cells (HSCs) can self-renew and also give rise to the entire repertoire of hematopoietic cells. During acute infectious and inflammatory stresses, the hematopoietic system can quickly adapt to demand by increasing output of innate immune cells many-fold, often at the expense of lymphopoiesis and erythropoiesis. We review recent advances in understanding the regulation of stress-induced hematopoiesis with a specific focus on the direct effects of inflammatory signaling on hematopoietic stem and progenitor cells (HSPCs). Recent findings Recent studies have highlighted several areas of exciting new developments in the field, including the complex interaction and crosstalk within HSPCs and between bone marrow mesenchymal stem cells and endothelial cells needed to achieve regulated myelopoiesis, identification of increased number of inflammatory and infectious molecules with direct effects on HSPCs, the critical role of inflammatory signaling on embryonic specification of HSCs, and the ability of cytokines to instruct lineage choice at the HSPC level. Summary These exciting new findings will shape our fundamental understanding of how inflammatory signaling regulates hematopoiesis in health and disease, and facilitate the development of potential interventions to treat hematologic diseases associated with altered inflammatory signaling.

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Section: Regulation Of Stress-induced Hematopoiesis By Cytokine Signamentioning

confidence: 99%

Regulation of stress-induced hematopoiesis

Zhao

Baltimore²

2015

Current Opinion in Hematology

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“…Further studies confirm a role of TGF-β signaling pathways in modulating HSC quiescence (Yamazaki et al, 2009), partly by preventing reentry into the cell cycle (Logsdon et al, 2007). Recent data provide a paradigm for TGF-β signaling in regulating the balance between lymphoid-and myeloid-derived HSCs, leading to HSC aging (Quéré et al, 2014).…”

Section: Aging and Cancer Development: Signaling Pathways At The Inmentioning

confidence: 72%

Is the secret for a successful aging to keep track of cancer pathways?

Tramontano

Amicis

2018

Journal Cellular Physiology

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A successful aging could be gained by life satisfaction, social functioning, or psychological resources and, definitely, by increasing resistance to diverse age-related pathologies. Nowadays, cancer can be considered an age-related disease since the incidence of most cancers increases with age, rising more rapidly beginning in midlife. Although adults with extended longevity are less likely to develop cancer, it is now emerging that aging and cancer share common molecular links, and thus targeting these mechanisms may be suitable to treat multiple disorders, for the prolonging of healthy aging. At present, one of the cornerstones of antiaging is hormone-replacement therapy to treat diseases associated with a state of age-related sex-hormone deficiency in women and men; however, many studies question the relationship of hormone replacement to cancer recurrence. Here, we discuss signaling and metabolic molecular crossroad linking aging and cancer. This is useful to argue about the current knowledge of prolongevity and druggable targets and to motivate specific intervention strategies that could modify practices of the aging population, activating multiple longevity pathways but keeping track of cancer pathways, thereby potentially preserving health status.

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“…Another gene belonging to bromo-domain family is TRIM33, a transcriptional repressor with a role in cell proliferation. TRIM33 is a multifunctional protein implicated in TGFb signaling and hematopoietic stem cell [HSC] aging by regulating the balance between lymphoid and myeloid derived HSCs (29). In mice lacking TRIM33 premature hematopoietic aging has been implicated in predisposition to myeloproliferative disease as CML.…”

Section: Discussionmentioning

confidence: 99%

Clinical significance ofin vivocytarabine-induced gene expression signature in AML

Lamba

Pounds

Cao

et al. 2015

Leukemia & Lymphoma

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Despite initial remission, approximately 60-70% of adult and 30% of pediatric patients experience relapse or refractory AML. Studies so far have identified base line gene expression profiles of pathogenic and prognostic significance in AML, however extent of change in gene expression post-initiation of treatment has not been investigated. Exposure of leukemic cells to chemotherapeutic agents such as cytarabine, a mainstay of AML chemotherapy can trigger adaptive response by influencing leukemic cell transcriptome and hence development of resistance or refractory disease. It is however challenging to perform such a study due to lack of availability of specimens post-drug treatment. In this study our primary objective was to identify in vivo cytarabine induced changes in leukemia cell transcriptome and to evaluate their impact on clinical outcome. Our results highlight genes relevant to cytarabine resistance and support the concept of targeting cytarabine-induced genes as a means of improving response.

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Tif1γ regulates the TGF-β1 receptor and promotes physiological aging of hematopoietic stem cells

Cited by 62 publications

References 45 publications

Regulation of stress-induced hematopoiesis

Regulation of stress-induced hematopoiesis

Is the secret for a successful aging to keep track of cancer pathways?

Clinical significance ofin vivocytarabine-induced gene expression signature in AML

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