Loss of SIRT1 inhibits hematopoietic stem cell aging and age-dependent mixed phenotype acute leukemia

Aging of hematopoietic stem cells (HSCs) is linked to various blood disorders and malignancies. SIRT1 has been implicated in healthy aging, but its role in HSC aging is poorly understood. Surprisingly, we found that Sirt1 knockout improved the maintenance of quiescence of aging HSCs and their functi...

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Published inCommunications biology Vol. 5; no. 1; pp. 396 - 15
Main Authors Wang, Zhiqiang, Zhang, Chunxiao, Warden, Charles David, Liu, Zheng, Yuan, Yate-Ching, Guo, Chao, Wang, Charles, Wang, Jinhui, Wu, Xiwei, Ermel, Richard, Vonderfecht, Steven L., Wang, Xiuli, Brown, Christine, Forman, Stephen, Yang, Yaling, James You, M., Chen, WenYong
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 28.04.2022
Nature Publishing Group
Nature Portfolio
Subjects
13/100
13/109
13/2
13/31
13/89
14/63
38/77
42/41
45/22
45/29
45/90
631/532/2118/1542
631/532/7
692/4028/67/1990/283/1897
82/29
Aging
Aging - genetics
Animals
Biology
Biomedical and Life Sciences
Bone marrow
Bone marrow transplantation
Genotype & phenotype
Hematological diseases
Hematopoietic stem cells
Hematopoietic Stem Cells - metabolism
Leukemia
Leukemia - genetics
Leukemia - metabolism
Life Sciences
Mice
Oxidative metabolism
Phenotype
Phenotypes
Protein biosynthesis
Protein turnover
SIRT1 protein
Sirtuin 1 - genetics
Sirtuin 1 - metabolism
Stem cell transplantation
Stem cells
Therapeutic targets
Transcription factors
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Abstract Aging of hematopoietic stem cells (HSCs) is linked to various blood disorders and malignancies. SIRT1 has been implicated in healthy aging, but its role in HSC aging is poorly understood. Surprisingly, we found that Sirt1 knockout improved the maintenance of quiescence of aging HSCs and their functionality as well as mouse survival in serial bone marrow transplantation (BMT) recipients. The majority of secondary and tertiary BMT recipients of aging wild type donor cells developed B/myeloid mixed phenotype acute leukemia (MPAL), which was markedly inhibited by Sirt1 knockout. SIRT1 inhibition also reduced the growth and survival of human B/myeloid MPAL cells. Sirt1 knockout suppressed global gene activation in old HSCs, prominently the genes regulating protein synthesis and oxidative metabolism, which may involve multiple downstream transcriptional factors. Our results demonstrate an unexpected role of SIRT1 in promoting HSC aging and age-dependent MPAL and suggest SIRT1 may be a new therapeutic target for modulating functions of aging HSCs and treatment of MPAL. Studies employing serial bone marrow transplantation in mice show that Sirt1 knockout improves quiescence maintenance and function of aging hematopoietic stem cells. Sirt1 loss also prevents the development of age-dependent B/myeloid mixed phenotype acute leukemia.
AbstractList Aging of hematopoietic stem cells (HSCs) is linked to various blood disorders and malignancies. SIRT1 has been implicated in healthy aging, but its role in HSC aging is poorly understood. Surprisingly, we found that Sirt1 knockout improved the maintenance of quiescence of aging HSCs and their functionality as well as mouse survival in serial bone marrow transplantation (BMT) recipients. The majority of secondary and tertiary BMT recipients of aging wild type donor cells developed B/myeloid mixed phenotype acute leukemia (MPAL), which was markedly inhibited by Sirt1 knockout. SIRT1 inhibition also reduced the growth and survival of human B/myeloid MPAL cells. Sirt1 knockout suppressed global gene activation in old HSCs, prominently the genes regulating protein synthesis and oxidative metabolism, which may involve multiple downstream transcriptional factors. Our results demonstrate an unexpected role of SIRT1 in promoting HSC aging and age-dependent MPAL and suggest SIRT1 may be a new therapeutic target for modulating functions of aging HSCs and treatment of MPAL.Studies employing serial bone marrow transplantation in mice show that Sirt1 knockout improves quiescence maintenance and function of aging hematopoietic stem cells. Sirt1 loss also prevents the development of age-dependent B/myeloid mixed phenotype acute leukemia.
Studies employing serial bone marrow transplantation in mice show that Sirt1 knockout improves quiescence maintenance and function of aging hematopoietic stem cells. Sirt1 loss also prevents the development of age-dependent B/myeloid mixed phenotype acute leukemia.
Aging of hematopoietic stem cells (HSCs) is linked to various blood disorders and malignancies. SIRT1 has been implicated in healthy aging, but its role in HSC aging is poorly understood. Surprisingly, we found that Sirt1 knockout improved the maintenance of quiescence of aging HSCs and their functionality as well as mouse survival in serial bone marrow transplantation (BMT) recipients. The majority of secondary and tertiary BMT recipients of aging wild type donor cells developed B/myeloid mixed phenotype acute leukemia (MPAL), which was markedly inhibited by Sirt1 knockout. SIRT1 inhibition also reduced the growth and survival of human B/myeloid MPAL cells. Sirt1 knockout suppressed global gene activation in old HSCs, prominently the genes regulating protein synthesis and oxidative metabolism, which may involve multiple downstream transcriptional factors. Our results demonstrate an unexpected role of SIRT1 in promoting HSC aging and age-dependent MPAL and suggest SIRT1 may be a new therapeutic target for modulating functions of aging HSCs and treatment of MPAL. Studies employing serial bone marrow transplantation in mice show that Sirt1 knockout improves quiescence maintenance and function of aging hematopoietic stem cells. Sirt1 loss also prevents the development of age-dependent B/myeloid mixed phenotype acute leukemia.
Aging of hematopoietic stem cells (HSCs) is linked to various blood disorders and malignancies. SIRT1 has been implicated in healthy aging, but its role in HSC aging is poorly understood. Surprisingly, we found that Sirt1 knockout improved the maintenance of quiescence of aging HSCs and their functionality as well as mouse survival in serial bone marrow transplantation (BMT) recipients. The majority of secondary and tertiary BMT recipients of aging wild type donor cells developed B/myeloid mixed phenotype acute leukemia (MPAL), which was markedly inhibited by Sirt1 knockout. SIRT1 inhibition also reduced the growth and survival of human B/myeloid MPAL cells. Sirt1 knockout suppressed global gene activation in old HSCs, prominently the genes regulating protein synthesis and oxidative metabolism, which may involve multiple downstream transcriptional factors. Our results demonstrate an unexpected role of SIRT1 in promoting HSC aging and age-dependent MPAL and suggest SIRT1 may be a new therapeutic target for modulating functions of aging HSCs and treatment of MPAL.
Aging of hematopoietic stem cells (HSCs) is linked to various blood disorders and malignancies. SIRT1 has been implicated in healthy aging, but its role in HSC aging is poorly understood. Surprisingly, we found that Sirt1 knockout improved the maintenance of quiescence of aging HSCs and their functionality as well as mouse survival in serial bone marrow transplantation (BMT) recipients. The majority of secondary and tertiary BMT recipients of aging wild type donor cells developed B/myeloid mixed phenotype acute leukemia (MPAL), which was markedly inhibited by Sirt1 knockout. SIRT1 inhibition also reduced the growth and survival of human B/myeloid MPAL cells. Sirt1 knockout suppressed global gene activation in old HSCs, prominently the genes regulating protein synthesis and oxidative metabolism, which may involve multiple downstream transcriptional factors. Our results demonstrate an unexpected role of SIRT1 in promoting HSC aging and age-dependent MPAL and suggest SIRT1 may be a new therapeutic target for modulating functions of aging HSCs and treatment of MPAL.
Aging of hematopoietic stem cells (HSCs) is linked to various blood disorders and malignancies. SIRT1 has been implicated in healthy aging, but its role in HSC aging is poorly understood. Surprisingly, we found that Sirt1 knockout improved the maintenance of quiescence of aging HSCs and their functionality as well as mouse survival in serial bone marrow transplantation (BMT) recipients. The majority of secondary and tertiary BMT recipients of aging wild type donor cells developed B/myeloid mixed phenotype acute leukemia (MPAL), which was markedly inhibited by Sirt1 knockout. SIRT1 inhibition also reduced the growth and survival of human B/myeloid MPAL cells. Sirt1 knockout suppressed global gene activation in old HSCs, prominently the genes regulating protein synthesis and oxidative metabolism, which may involve multiple downstream transcriptional factors. Our results demonstrate an unexpected role of SIRT1 in promoting HSC aging and age-dependent MPAL and suggest SIRT1 may be a new therapeutic target for modulating functions of aging HSCs and treatment of MPAL.Aging of hematopoietic stem cells (HSCs) is linked to various blood disorders and malignancies. SIRT1 has been implicated in healthy aging, but its role in HSC aging is poorly understood. Surprisingly, we found that Sirt1 knockout improved the maintenance of quiescence of aging HSCs and their functionality as well as mouse survival in serial bone marrow transplantation (BMT) recipients. The majority of secondary and tertiary BMT recipients of aging wild type donor cells developed B/myeloid mixed phenotype acute leukemia (MPAL), which was markedly inhibited by Sirt1 knockout. SIRT1 inhibition also reduced the growth and survival of human B/myeloid MPAL cells. Sirt1 knockout suppressed global gene activation in old HSCs, prominently the genes regulating protein synthesis and oxidative metabolism, which may involve multiple downstream transcriptional factors. Our results demonstrate an unexpected role of SIRT1 in promoting HSC aging and age-dependent MPAL and suggest SIRT1 may be a new therapeutic target for modulating functions of aging HSCs and treatment of MPAL.
ArticleNumber 396
Author Wang, Zhiqiang
Ermel, Richard
Wang, Xiuli
Brown, Christine
Zhang, Chunxiao
Yang, Yaling
Yuan, Yate-Ching
Guo, Chao
Warden, Charles David
Wu, Xiwei
Chen, WenYong
Wang, Charles
Liu, Zheng
James You, M.
Wang, Jinhui
Vonderfecht, Steven L.
Forman, Stephen
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Snippet Aging of hematopoietic stem cells (HSCs) is linked to various blood disorders and malignancies. SIRT1 has been implicated in healthy aging, but its role in HSC...
Studies employing serial bone marrow transplantation in mice show that Sirt1 knockout improves quiescence maintenance and function of aging hematopoietic stem...
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Aging
Aging - genetics
Animals
Biology
Biomedical and Life Sciences
Bone marrow
Bone marrow transplantation
Genotype & phenotype
Hematological diseases
Hematopoietic stem cells
Hematopoietic Stem Cells - metabolism
Leukemia
Leukemia - genetics
Leukemia - metabolism
Life Sciences
Mice
Oxidative metabolism
Phenotype
Phenotypes
Protein biosynthesis
Protein turnover
SIRT1 protein
Sirtuin 1 - genetics
Sirtuin 1 - metabolism
Stem cell transplantation
Stem cells
Therapeutic targets
Transcription factors
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Title Loss of SIRT1 inhibits hematopoietic stem cell aging and age-dependent mixed phenotype acute leukemia
URI https://link.springer.com/article/10.1038/s42003-022-03340-w
https://www.ncbi.nlm.nih.gov/pubmed/35484199
https://www.proquest.com/docview/2656454728
https://www.proquest.com/docview/2658232719
https://pubmed.ncbi.nlm.nih.gov/PMC9051098
https://doaj.org/article/9d0e1dc32e3944ccbb5ec887342c8d2e
Volume 5
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