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Journal articles on the topic 'Stress hematopoiesis'

Author: Grafiati

Published: 24 May 2025

Last updated: 31 July 2025

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1

Link, Daniel C. "Clonal Evolution During Stress Hematopoiesis." Blood 130, Suppl_1 (2017): SCI—38—SCI—38. http://dx.doi.org/10.1182/blood.v130.suppl_1.sci-38.sci-38.

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Hematopoietic stem and progenitor cells (HSPCs) acquire somatic mutations with age resulting in a heterogeneous cell population, with each HSPC possessing its own unique set of private mutations. HSPCs that acquire somatic mutations that confer a competitive fitness advantage relative to their normal counterparts may clonally expand. Indeed, several groups have documented the presence of clonal hematopoiesis in healthy individuals. Although originally thought to be limited to older individuals, a recent study using an ultra-sensitive sequencing technique showed that expanded hematopoietic clon

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2

Chen, Ying-Ying, Yu-Feng Liu, Yong-Dong Liu, Xiao-Hui Deng, and Jie Zhou. "IRF7 suppresses hematopoietic regeneration under stress via CXCR4." Stem Cells 39, no. 2 (2020): 183–95. http://dx.doi.org/10.1002/stem.3308.

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Abstract Hematopoietic stem cells (HSCs) maintain quiescence under steady state; however, they are compelled to proliferate and expand to replenish the blood system under stress. The molecular basis underlying stress hematopoiesis remains to be fully understood. In this study, we reported that IRF7 represents an important regulator of stress hematopoiesis. Interferon regulatory factor 7 (IRF7) was dispensable for normal hematopoiesis, whereas its deficiency significantly enhanced hematopoietic stem and progenitor cells (HSPCs) regeneration and improved long-term repopulation of HSCs under stre

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3

Watt, Suzanne M., and Maria G. Roubelakis. "Deciphering the Complexities of Adult Human Steady State and Stress-Induced Hematopoiesis: Progress and Challenges." International Journal of Molecular Sciences 26, no. 2 (2025): 671. https://doi.org/10.3390/ijms26020671.

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Human hematopoietic stem cells (HSCs) have traditionally been viewed as self-renewing, multipotent cells with enormous potential in sustaining essential steady state blood and immune cell production throughout life. Indeed, around 86% (1011–1012) of new cells generated daily in a healthy young human adult are of hematopoietic origin. Therapeutically, human HSCs have contributed to over 1.5 million hematopoietic cell transplants (HCTs) globally, making this the most successful regenerative therapy to date. We will commence this review by briefly highlighting selected key achievements (from 1868

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4

Wu, Jiang, Weiwei Zhang, Qian Ran, et al. "The Differentiation Balance of Bone Marrow Mesenchymal Stem Cells Is Crucial to Hematopoiesis." Stem Cells International 2018 (2018): 1–13. http://dx.doi.org/10.1155/2018/1540148.

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Bone marrow mesenchymal stem cells (BMSCs), the important component and regulator of bone marrow microenvironment, give rise to hematopoietic-supporting stromal cells and form hematopoietic niches for hematopoietic stem cells (HSCs). However, how BMSC differentiation affects hematopoiesis is poorly understood. In this review, we focus on the role of BMSC differentiation in hematopoiesis. We discussed the role of BMSCs and their progeny in hematopoiesis. We also examine the mechanisms that cause differentiation bias of BMSCs in stress conditions including aging, irradiation, and chemotherapy. M

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5

Tseng, Yu-Jung, Richard Chapple, Tianyuan Hu, et al. "Hematopoietic Hierarchy Under Steady-State and Stress Conditions." Blood 134, Supplement_1 (2019): 1181. http://dx.doi.org/10.1182/blood-2019-125110.

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The maintenance of the hematopoietic system by hematopoietic stem cells (HSCs) is an important topic in both clinical and basic hematology study due to their enormous therapeutic potential. The hematopoietic hierarchy has recently garnered renewed interest following the development of single-cell assays and improved strategies for genetic labeling, resulting in new hierarchical models that challenge the classical view of hematopoiesis. However, the kinetic of hematopoiesis under steady-state and stress condition and the contribution of HSCs toward steady-state hematopoiesis remain controversia

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6

Karlsson, Stefan. "Stress hematopoiesis requires Erg." Blood 118, no. 9 (2011): 2379–80. http://dx.doi.org/10.1182/blood-2011-07-362699.

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7

Suda, Toshio. "Hematopoiesis under the stress." Experimental Hematology 42, no. 8 (2014): S2. http://dx.doi.org/10.1016/j.exphem.2014.07.004.

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8

Essers, Marieke. "Inflammation-induced stress hematopoiesis." Experimental Hematology 53 (September 2017): S28. http://dx.doi.org/10.1016/j.exphem.2017.06.017.

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9

Landspersky, Theresa, Mehmet Saçma, Jennifer Rivière, et al. "Autophagy in mesenchymal progenitors protects mice against bone marrow failure after severe intermittent stress." Blood 139, no. 5 (2022): 690–703. http://dx.doi.org/10.1182/blood.2021011775.

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Abstract The cellular mechanisms required to ensure homeostasis of the hematopoietic niche and the ability of this niche to support hematopoiesis upon stress remain elusive. We here identify Wnt5a in Osterix+ mesenchymal progenitor and stem cells (MSPCs) as a critical factor for niche-dependent hematopoiesis. Mice lacking Wnt5a in MSPCs suffer from stress-related bone marrow (BM) failure and increased mortality. Niche cells devoid of Wnt5a show defective actin stress fiber orientation due to an elevated activity of the small GTPase CDC42. This results in incorrect positioning of autophagosomes

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10

Brenet, Fabienne A., Pouneh Kermani, Shahin Rafii та Joseph M. Scandura. "TGFβ Restores Hematopoietic Homeostasis After Chemotherapy." Blood 120, № 21 (2012): 2344. http://dx.doi.org/10.1182/blood.v120.21.2344.2344.

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Abstract Abstract 2344 Background: Hematopoietic stem cells (HSCs) are required for lifelong blood cell production and, to prevent exhaustion, the majority of HSCs are deeply quiescent during steady-state hematopoiesis. Paracrine factors produced by specialized bone marrow niche cells maintain HSC quiescence. Yet, evolution demands a rapid hematopoietic response to stressors such as infection, bleeding or toxin exposure. These triggers set off a remarkable adaptation in hematopoiesis that sacrifices HSPC quiescence, and the protection it affords, to meet an urgent need for new blood cell produ

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11

Migliaccio, Anna Rita, Fabrizio Martelli, Maria Verrucci, et al. "Gata1 expression driven by the alternative HS2 enhancer in the spleen rescues the hematopoietic failure induced by the hypomorphic Gata1low mutation." Blood 114, no. 10 (2009): 2107–20. http://dx.doi.org/10.1182/blood-2009-03-211680.

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Abstract Rigorously defined reconstitution assays developed in recent years have allowed recognition of the delicate relationship that exists between hematopoietic stem cells and their niches. This balance ensures that hematopoiesis occurs in the marrow under steady-state conditions. However, during development, recovery from hematopoietic stress and in myeloproliferative disorders, hematopoiesis occurs in extramedullary sites whose microenvironments are still poorly defined. The hypomorphic Gata1low mutation deletes the regulatory sequences of the gene necessary for its expression in hematopo

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12

Lozano, Guillermina (Gigi). "p53-Mediated Stress and Tissue-Dependent Cell Fate Decisions; Implications for p53 Targeting." Blood 118, no. 21 (2011): SCI—3—SCI—3. http://dx.doi.org/10.1182/blood.v118.21.sci-3.sci-3.

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Abstract Abstract SCI-3 The activity of the p53 tumor suppressor is tightly regulated by Mdm2, an E3 ubiquitin ligase that targets p53 for degradation. Loss of Mdm2 in embryos or in individual tissues in vivo results in cell lethal events that are p53-dependent. A hypomorphic allele of p53, p53515C (encoding the p53R172P protein), rescues the embryonic lethality of Mdm2–/– mice. Mdm2–/– p53515C/515C mice, however, die by postnatal day 13 due to hematopoietic failure. In these mice, hematopoiesis is normal during embryogenesis. After birth, these mice had elevated reactive oxygen species (ROS),

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13

Brenet, Fabienne A., and Joseph M. Scandura. "CDKN1C Modulates the Stress-Reponse of Hematopoietic Stem Cells Rendering Hematopoiesis Resistant to Chemotherapeutics." Blood 116, no. 21 (2010): 3162. http://dx.doi.org/10.1182/blood.v116.21.3162.3162.

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Abstract Abstract 3162 The cyclin-dependent kinase inhibitor (CDKI) CDKN1C (p57) is a tumor suppressor gene with strong differential expression in both human and murine hematopoietic stem cells (HSC). Whereas the expression of other CDKIs is normal in most hematopoietic malignancies, p57 expression is silenced in 30 to 55% of acute lymphoblastic leukemia (ALL), acute myelogenous leukemia (AML), and B-Cell lymphoma patients suggesting a role as suppressor of hematopoietic cell transformation. p57 has a unique role in embryogenesis functioning in tissue-specific developmental programs to coordin

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14

Fielding, Claire, and Simón Méndez-Ferrer. "Neuronal regulation of bone marrow stem cell niches." F1000Research 9 (June 16, 2020): 614. http://dx.doi.org/10.12688/f1000research.22554.1.

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The bone marrow (BM) is the primary site of postnatal hematopoiesis and hematopoietic stem cell (HSC) maintenance. The BM HSC niche is an essential microenvironment which evolves and responds to the physiological demands of HSCs. It is responsible for orchestrating the fate of HSCs and tightly regulates the processes that occur in the BM, including self-renewal, quiescence, engraftment, and lineage differentiation. However, the BM HSC niche is disturbed following hematological stress such as hematological malignancies, ionizing radiation, and chemotherapy, causing the cellular composition to a

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15

Priestley, Gregory V., Linda M. Scott, Tatiana Ulyanova та Thalia Papayannopoulou. "Lack of α4 integrin expression in stem cells restricts competitive function and self-renewal activity". Blood 107, № 7 (2006): 2959–67. http://dx.doi.org/10.1182/blood-2005-07-2670.

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AbstractAlpha4 integrin or VLA4 (CD49d/CD29) is a multitask molecule with wide expression within and outside the hematopoietic system. Because targeted ablation of α4 integrin leads to embryonic lethality, to study its effects on adult hematopoiesis, we used animals with conditional excision of α4 integrin (α4Δ/Δ) in hematopoietic cells. In such animals, we previously documented weakened bone marrow retention of progenitor cells during homeostasis and impaired homing and short-term engraftment after transplantation. In the present study we show that long-term repopulating cells lacking α4 inte

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16

Unnisa, Zeenath, Jason P. Clark, Jayeeta Roychoudhury, et al. "Meis1 preserves hematopoietic stem cells in mice by limiting oxidative stress." Blood 120, no. 25 (2012): 4973–81. http://dx.doi.org/10.1182/blood-2012-06-435800.

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Abstract The transcription factor Meis1 is expressed preferentially in hematopoietic stem cells (HSCs) and overexpressed in certain leukemias. However, the functions of Meis1 in hematopoiesis remain largely unknown. In the present study, we found that Meis1 is required for the maintenance of hematopoiesis under stress and over the long term, whereas steady-state hematopoiesis was sustained in the absence of Meis1 in inducible knock-out mice. BM cells of Meis1-deficient mice showed reduced colony formation and contained significantly fewer numbers of long-term HSCs, which exhibited loss of quie

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17

Pucella, Joseph N., Samik Upadhaya, and Boris Reizis. "The Source and Dynamics of Adult Hematopoiesis: Insights from Lineage Tracing." Annual Review of Cell and Developmental Biology 36, no. 1 (2020): 529–50. http://dx.doi.org/10.1146/annurev-cellbio-020520-114601.

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The generation of all blood cell lineages (hematopoiesis) is sustained throughout the entire life span of adult mammals. Studies using cell transplantation identified the self-renewing, multipotent hematopoietic stem cells (HSCs) as the source of hematopoiesis in adoptive hosts and delineated a hierarchy of HSC-derived progenitors that ultimately yield mature blood cells. However, much less is known about adult hematopoiesis as it occurs in native hosts, i.e., without transplantation. Here we review recent advances in our understanding of native hematopoiesis, focusing in particular on the app

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18

Zhao, Jimmy L., and David Baltimore. "Regulation of stress-induced hematopoiesis." Current Opinion in Hematology 22, no. 4 (2015): 286–92. http://dx.doi.org/10.1097/moh.0000000000000149.

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19

Anderson, Georgina A., Melanie Rodriguez, and Katie L. Kathrein. "Regulation of stress-induced hematopoiesis." Current Opinion in Hematology 27, no. 4 (2020): 279–87. http://dx.doi.org/10.1097/moh.0000000000000589.

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20

Thompson, Zanshé, Georgina A. Anderson, Seth Gabriel, Melanie Rodriguez, Vera Binder, and Katie L. Kathrein. "Ing4-Deficiency Enhances Hematopoietic Stem Cell Quiescence and Confers Resistance to Inflammatory Stress." Blood 138, Supplement 1 (2021): 1095. http://dx.doi.org/10.1182/blood-2021-154353.

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Abstract In a screen for epigenetic regulators of hematopoiesis in zebrafish, we identified a requirement of the tumor suppressor protein, Ing4, in hematopoietic stem and progenitor cell (HSPC) specification. Though the Ing4 mechanism of action remains poorly characterized, loss of Ing4 has been shown to promote stem cell-like characteristics in malignant cells and it is a frequent target of inactivation in various types of cancer. Mutations in Ing4 cause deregulation of both NF-kB and c-Myc target gene expression. We have also identified a requirement for Ing4 in murine hematopoiesis. Ing4-/-

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21

Cao, Yu-An, Amy J. Wagers, Holger Karsunky, et al. "Heme Oxygenase 1 Deficiency Compromises Stress Responses of Hematopoietic Stem Cells." Blood 108, no. 11 (2006): 1353. http://dx.doi.org/10.1182/blood.v108.11.1353.1353.

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Abstract Hematopoietic stem cells (HSCs) must be able to balance their self-renewal and differentiation activities in order to preserve their compartment in response to hematopoietic insults for efficient and life-long hematopoiesis while ensuring sufficient blood production to meet the increased hematopoietic demand. Mechanism(s) that regulate this balance during stress hematopoiesis remain to be fully understood. Heme oxygenase 1 (HO-1) is an important stress-inducible protein and a key enzyme of heme degradation that produces iron, bilirubin, and carbon monoxide (CO). CO is a gaseous regula

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22

Xiao, Nan, Kaushal Jani, Kelly Morgan, et al. "Hematopoietic stem cells lacking Ott1 display aspects associated with aging and are unable to maintain quiescence during proliferative stress." Blood 119, no. 21 (2012): 4898–907. http://dx.doi.org/10.1182/blood-2012-01-403089.

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Abstract Aging degrades hematopoietic stem cell (HSC) functions, including stress response; however, the involved molecular pathways are incompletely defined. Murine BM conditionally deleted for One-Twenty-Two-1 (Ott1), is able to maintain lifelong hematopoiesis and has preserved numbers of long-term HSCs, yet cannot repopulate nor sustain itself after transplantation against a competitor even when Ott1 is excised after engraftment. We show, specifically under replicative stress, that Ott1-deleted HSCs have a significant reduction of the G0 cell-cycle fraction associated with self-renewal and

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23

Wang, Nan, Jing Yin, Yangyang Zhao, et al. "Twist1 is Essential for Hematopoietic Stem Cell Maintenance and Stress Hematopoiesis." Experimental Hematology 64 (August 2018): S110. http://dx.doi.org/10.1016/j.exphem.2018.06.173.

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24

Daria, Deidre, Marie-Dominique Filippi, Erik S. Knudsen, et al. "The retinoblastoma tumor suppressor is a critical intrinsic regulator for hematopoietic stem and progenitor cells under stress." Blood 111, no. 4 (2008): 1894–902. http://dx.doi.org/10.1182/blood-2007-02-071746.

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The retinoblastoma tumor suppressor protein (RB) plays important roles in the control of the cell division cycle. It is estimated that RB is dysfunctional/inactivated in up to 40% of human leukemias. The consequences of loss of RB on hematopoietic stem and progenitor cell (HSPC) function in vivo are incompletely understood. Here, we report that mice genetically deficient in Rb in all hematopoietic cells (Vav-Cre Rb knockout [KO] animals) showed altered contribution of distinct hematopoietic cell lineages to peripheral blood, bone marrow, and spleen; significantly increased extramedullary hemat

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25

Thompson, Zanshe, Melanie Rodriguez, Seth Gabriel, et al. "Ing4 Regulates Stress Hematopoiesis and Represses Self-Renewal in Multipotent Progenitor Cells." Blood 134, Supplement_1 (2019): 724. http://dx.doi.org/10.1182/blood-2019-129054.

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Hematopoiesis is tightly regulated by a network of transcription factors and complexes that are required for the maintenance and development of HSCs. In a screen for epigenetic regulators of hematopoiesis in zebrafish, we identified a requirement of the tumor suppressor protein, Ing4, in hematopoietic stem and progenitor cell (HSPC) specification. Though the Ing4 mechanism of action remains poorly characterized, it has been shown to promote stem-like cell characteristics in malignant cells and is a frequent target of inactivation in various cancer types. The tumor suppressive activity is, in p

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26

Karigane, Daiki, Keiyo Takubo, Shinichiro Okamoto та Toshio Suda. "p38α Is Required for Proper Proliferation of Hematopoietic Stem Cells during Stress". Blood 124, № 21 (2014): 4317. http://dx.doi.org/10.1182/blood.v124.21.4317.4317.

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Abstract Hematopoietic stem cells (HSCs) are capable of self-renewal and multilineage-differentiation during lifespan. HSCs are maintained in a quiescent state to avoid cellular senescence. Previous reports utilizing pharmacological inhibitors or shRNAs against p38MAPK suggest a pivotal role of p38MAPK-pRb-Ink4a signaling in induction of HSC senescence by hematological stress or chronological aging. However, no genetic evidence exists for p38MAPK-mediated cellular senescence in vivo. Here we report unexpected roles of the dominant isoform of p38MAPK family, p38α, in adult hematological system.

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27

Leimkühler, Nils B., and Rebekka K. Schneider. "Inflammatory bone marrow microenvironment." Hematology 2019, no. 1 (2019): 294–302. http://dx.doi.org/10.1182/hematology.2019000045.

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Abstract Self-renewing hematopoietic stem cells and their progeny, lineage-specific downstream progenitors, maintain steady-state hematopoiesis in the bone marrow (BM). Accumulating evidence over the last few years indicates that not only primitive hematopoietic stem and progenitor cells (HSPCs), but also cells defining the microenvironment of the BM (BM niche), sense hematopoietic stress signals. They respond by directing and orchestrating hematopoiesis via not only cell-intrinsic but also cell-extrinsic mechanisms. Inflammation has many beneficial roles by activating the immune system in tis

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28

Borghesi, Lisa A., Ailing Liu, and Ying Ding. "Compromised emergency hematopoiesis in obesity requires TLR4." Journal of Immunology 196, no. 1_Supplement (2016): 52.18. http://dx.doi.org/10.4049/jimmunol.196.supp.52.18.

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Abstract Following acute injury/infection, bone marrow (BM) precursors must responsively redirect from steady-state to emergency hematopoiesis. Prospective and retrospective studies establish obesity as risk factor for infection but the mechanisms are poorly understood. Here, we show in a murine model of obesity that moderate changes in steady-state BM hematopoiesis become exaggerated during hematopoietic duress. At steady-state, diet-induced obese mice have a 30% decrease in BM hematopoietic stem cells (HSCs) with a parallel increase in splenic HSCs. HSCs are functionally competent in vitro a

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29

Robert, Tom. "Mitochondrial Dysfunction and Hematopoietic Impairment in Diabetes: The Oxidative Stress Connection." RESEARCH INVENTION JOURNAL OF SCIENTIFIC AND EXPERIMENTAL SCIENCES 5, no. 2 (2025): 1–7. https://doi.org/10.59298/rijses/2025/521700.

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Diabetes mellitus (DM) is a chronic metabolic disorder characterized by persistent hyperglycemia, which leads to systemic complications. Among these, mitochondrial dysfunction plays a critical role in hematopoietic impairment, primarily through the induction of oxidative stress. The mitochondrial electron transport chain (ETC) is a significant source of reactive oxygen species (ROS) in diabetes, leading to oxidative damage in hematopoietic stem and progenitor cells (HSPCs). This review explores the intricate relationship between mitochondrial dysfunction, oxidative stress, and hematopoietic ab

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30

Li, Zhaofeng, Meng Su, Xinshu Xie, et al. "mDia formins form hetero-oligomers and cooperatively maintain murine hematopoiesis." PLOS Genetics 19, no. 12 (2023): e1011084. http://dx.doi.org/10.1371/journal.pgen.1011084.

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mDia formin proteins regulate the dynamics and organization of the cytoskeleton through their linear actin nucleation and polymerization activities. We previously showed that mDia1 deficiency leads to aberrant innate immune activation and induces myelodysplasia in a mouse model, and mDia2 regulates enucleation and cytokinesis of erythroblasts and the engraftment of hematopoietic stem and progenitor cells (HSPCs). However, whether and how mDia formins interplay and regulate hematopoiesis under physiological and stress conditions remains unknown. Here, we found that both mDia1 and mDia2 are requ

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31

Yura, Yoshimitsu, Emiri Miura-Yura, Yasufumi Katanasaka, et al. "The Cancer Therapy-Related Clonal Hematopoiesis Driver Gene Ppm1d Promotes Inflammation and Non-Ischemic Heart Failure in Mice." Circulation Research 129, no. 6 (2021): 684–98. http://dx.doi.org/10.1161/circresaha.121.319314.

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Rationale: Cancer therapy can be associated with short- and long-term cardiac dysfunction. Patients with cancer often exhibit therapy-related clonal hematopoiesis (t-CH), an aggressive form of clonal hematopoiesis that can result from somatic mutations in genes encoding regulators of the DNA-damage response (DDR) pathway. Gain-of-function mutations in exon 6 of the protein phosphatase Mg2+/Mn2+ dependent 1D ( PPM1D ) gene are the most frequently mutated DNA-damage response gene associated with t-CH. Whether t-CH can contribute to cardiac dysfunction is unknown. Objective: We evaluated the caus

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32

Lu, Wenyi, Kaiyan Liu, Weimin Wang, Shujuan Wang, and Yonghuai Feng. "Long-Term Treatment with Rosiglitazone Delays Hematopoietic Recovery in Response to Stress." Blood 126, no. 23 (2015): 4769. http://dx.doi.org/10.1182/blood.v126.23.4769.4769.

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Abstract Rosiglitazone is a peroxisome proliferator activated receptor-γ(PPAR-γ) agonist available to improve glucose metabolism in patients with Type 2 diabetes. Recent evidence suggests that therapeutic use of rosiglitazone have caused unwanted hematological side effects, such as anemia, leukopenia, thrombocytopenia, even pancytopenia. However, others reported that pretreatment with rosiglitazone for 5 days could protect against 5-Fu-induced myelotoxity which is FLT3 dependent. Thus, it is still unclear the exact effects of rosiglitazone treatment on homeostatic and stress hematopoiesis. Ros

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33

Li, June, Daniel P. Sejas, and Qishen Pang. "Nucleophosmin Regulates Differentiation, Cell Cycle Progression, and Stress Response in Hematopoietic Progenitor Cells." Blood 106, no. 11 (2005): 312. http://dx.doi.org/10.1182/blood.v106.11.312.312.

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Abstract Nucleophosmin (NPM) is a multifunctional protein frequently overexpressed in actively proliferating cells including tumor and hematopoietic stem cells. Strong evidence indicates that NPM is involved in hematopoiesis and leukemic development. Here we report that NPM enhances the proliferative potential of hematopoietic stem/progenitor cells and increases cell survival upon stress challenge. Specifically, lin-Sca1+c-kit+ bone marrow cells transduced with retroviral vector expressing NPM exhibited higher proliferative rates in both short-term liquid culture and clonogenic progenitor cell

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34

Cao, Yu-An, Amy J. Wagers, Holger Karsunky, et al. "Heme oxygenase-1 deficiency leads to disrupted response to acute stress in stem cells and progenitors." Blood 112, no. 12 (2008): 4494–502. http://dx.doi.org/10.1182/blood-2007-12-127621.

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Abstract An effective response to extreme hematopoietic stress requires an extreme elevation in hematopoiesis and preservation of hematopoietic stem cells (HSCs). These diametrically opposed processes are likely to be regulated by genes that mediate cellular adaptation to physiologic stress. Herein, we show that heme oxygenase-1 (HO-1), the inducible isozyme of heme degradation, is a key regulator of these processes. Mice lacking one allele of HO-1 (HO-1+/−) showed accelerated hematopoietic recovery from myelotoxic injury, and HO-1+/− HSCs repopulated lethally irradiated recipients with more r

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35

Macleod, Kay F. "Apoptosis and the DNA Damage Response: The Role of the RB Tumor Suppressor Pathway in Oxidative Stress Responses in the Hematopoietic System." Blood 114, no. 22 (2009): SCI—15—SCI—15. http://dx.doi.org/10.1182/blood.v114.22.sci-15.sci-15.

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Abstract Abstract SCI-15 Exposure to pro-oxidants and defects in repair of oxidative base damage is associated with disease and aging and also contributes to the development of anemia, bone marrow failure and hematopoietic malignancies. Our work examines the role of the RB tumor suppressor pathway in the response of the hematopoietic system to oxidative stress and DNA damage. Evidence from mouse models has identified a role for the Rb protein (pRb) in the regulation of hematopoiesis through cell intrinsic functions in blood cell types but also through effects on the bone marrow microenvironmen

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36

Zhang, Inga Hofmann, Elizabeth H. Stover, Dana E. Cullen, et al. "Hedgehog Signaling Is Dispensable for Adult Murine Hematopoiesis and Leukemogenesis." Blood 112, no. 11 (2008): 1391. http://dx.doi.org/10.1182/blood.v112.11.1391.1391.

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Abstract Hedgehog (Hh) pathway proteins are a highly conserved family of intracellular signaling molecules that are critical for the development of multiple organs and tissues, and play a role in cell fate determination of self-renewing tissues in the adult. Mutations that impair Hh signaling have been associated with developmental abnormalities, and recent studies indicate that Hh plays an important role in hemangioblast formation and in adult hematopoiesis, as well as in the differentiation and proliferation of hematopoietic stem cells (HSC) and progenitor cells. We used a genetic and pharma

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37

Thapa, Roshina, and Bibek Bhatta. "3205 – CANCEROUS IMPACT OF CHRONIC STRESS-HEMATOPOIESIS." Experimental Hematology 111 (2022): S147. http://dx.doi.org/10.1016/j.exphem.2022.07.261.

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38

Tew, Kenneth D. "Hematopoiesis, S-Glutathionylation and Stress Response Pathways." Free Radical Biology and Medicine 96 (July 2016): S10. http://dx.doi.org/10.1016/j.freeradbiomed.2016.04.051.

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39

Thapa, Roshina, and Bibek Bhatta. "3191 – CANCEROUS IMPACT OF CHRONIC STRESS-HEMATOPOIESIS." Experimental Hematology 124 (2023): S145. http://dx.doi.org/10.1016/j.exphem.2023.06.298.

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40

Morgan, Pooranee K., and Andrew J. Murphy. "Make hematopoiesis great again: countering oxidative stress!" Blood 145, no. 11 (2025): 1102–4. https://doi.org/10.1182/blood.2024027793.

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41

Mehta, Arnav, David Baltimore, and Jimmy Zhao. "microRNA-132 regulates hematopoietic stem cell function and survival through FOXO3a (HEM5P.226)." Journal of Immunology 194, no. 1_Supplement (2015): 120.6. http://dx.doi.org/10.4049/jimmunol.194.supp.120.6.

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Abstract A complex network of interactions tightly regulates hematopoiesis to ensure balanced and appropriate output of blood cells, both under normal and stressful conditions. This network includes a novel class of RNA molecules, called microRNAs, that do not code for proteins, but instead negatively regulate the expression of genes. These molecules serve as “fine-tuners” of gene expression, and when dysregulated, can drastically alter the balance of hematopoiesis, potentially leading to cancer. We have identified microRNA-132 to be enriched in certain hematopoietic progenitors, particularly

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Scortegagna, Marzia, Margaret A. Morris, Yavuz Oktay, Michael Bennett та Joseph A. Garcia. "The HIF family member EPAS1/HIF-2α is required for normal hematopoiesis in mice". Blood 102, № 5 (2003): 1634–40. http://dx.doi.org/10.1182/blood-2003-02-0448.

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AbstractHypoxic stress plays a role in pathophysiologic states such as myocardial infarction and cerebral vascular events as well as in normal physiologic conditions including development and hematopoiesis. Members of the hypoxia inducible factor (HIF) family function as transcriptional regulators of genes involved in the hypoxic response. After generating adult mice that globally lack endothelial PAS domain protein 1 (EPAS1, also known as HIF-2α/HRF/HLF/MOP3), the second member of the HIF family, characterization of the hematopoietic cell population indicated that the loss of EPAS1/HIF-2α res

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Krambs, Joseph R., Grazia Abou Ezzi, Juo-Chin Yao, Justin T. Li, and Daniel C. Link. "Canonical Signaling By TGF Family Members in Mesenchymal Stromal Cells Is Dispensable for Hematopoietic Niche Maintenance Under Basal and Stress Conditions." Blood 134, Supplement_1 (2019): 1209. http://dx.doi.org/10.1182/blood-2019-128693.

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The bone marrow contains a complex population of stromal and hematopoietic cells that together generate a unique microenvironment, or niche, to support hematopoiesis. Mesenchymal stromal cells are an important component of the bone marrow hematopoietic niche and include CXCL12-abundant reticular (CAR) cells, adipocytes, osteolineage cells, and arteriolar pericytes, all of which have been implicated in hematopoietic stem/progenitor cell (HSPC) maintenance. There also is evidence that adaptive changes in bone marrow stromal cells contributes to recovery from myelosuppresive therapy and the devel

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Wirth, Franziska, Alexander Lubosch, Stefan Hamelmann, and Inaam A. Nakchbandi. "Fibronectin and Its Receptors in Hematopoiesis." Cells 9, no. 12 (2020): 2717. http://dx.doi.org/10.3390/cells9122717.

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Fibronectin is a ubiquitous extracellular matrix protein that is produced by many cell types in the bone marrow and distributed throughout it. Cells of the stem cell niche produce the various isoforms of this protein. Fibronectin not only provides the cells a scaffold to bind to, but it also modulates their behavior by binding to receptors on the adjacent hematopoietic stem cells and stromal cells. These receptors, which include integrins such as α4β1, α9β1, α4β7, α5β1, αvβ3, Toll-like receptor-4 (TLR-4), and CD44, are found on the hematopoietic stem cell. Because the knockout of fibronectin i

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Kleppe, Maria, Matthew H. Spitzer, Sheng Li, et al. "JAK1 As a Convergent Regulator of Hematopoietic Stem Cell Function and Stress Hematopoiesis." Blood 128, no. 22 (2016): 722. http://dx.doi.org/10.1182/blood.v128.22.722.722.

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Abstract Cytokine-mediated signal transduction is critical to hematopoiesis, immune responses, and other physiological processes. Aberrant production and secretion of pro-inflammatory cytokines disturbs homeostasis and proper immune function and if persistent results in symptoms of chronic inflammation. Previous studies have illustrated the importance of JAK1 as an effector of cytokine signaling, including in immunological and neoplastic diseases such that selective JAK1 inhibition is currently being investigated in clinical trials. However, the role of Jak1 in hematopoietic stem cell (HSC) fu

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Kleppe, Maria, Matthew H. Spitzer, Sheng Li, et al. "Jak1 Integrates Cytokine Sensing to Regulate Hematopoietic Stem Cell Function and Stress Hematopoiesis." Cell Stem Cell 21, no. 4 (2017): 489–501. http://dx.doi.org/10.1016/j.stem.2017.08.011.

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Kleppe, Maria, Matthew H. Spitzer, Sheng Li, et al. "Jak1 Integrates Cytokine Sensing to Regulate Hematopoietic Stem Cell Function and Stress Hematopoiesis." Cell Stem Cell 22, no. 2 (2018): 277. http://dx.doi.org/10.1016/j.stem.2017.12.018.

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Scott, Linda M., Gregory V. Priestley та Thalia Papayannopoulou. "Deletion of α4 Integrins from Adult Hematopoietic Cells Reveals Roles in Homeostasis, Regeneration, and Homing". Molecular and Cellular Biology 23, № 24 (2003): 9349–60. http://dx.doi.org/10.1128/mcb.23.24.9349-9360.2003.

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ABSTRACT We have explored the functional implications of inducible α4 integrin deletion during adult hematopoiesis by generating a conditional-knockout mouse model, and we show that α4 integrin-deficient hematopoietic progenitor cells accumulate in the peripheral blood soon after interferon-induced gene deletion. Although their numbers gradually stabilize at a lower level, progenitor cell influx into the circulation continues at above-normal levels for more than 50 weeks. Concomitantly, a progressive accumulation of progenitors occurs within the spleen. In addition, the regeneration of erythro

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Asai, Takashi, Yan Liu, Silvana Di Giandomenico, et al. "Necdin, a p53 target gene, regulates the quiescence and response to genotoxic stress of hematopoietic stem/progenitor cells." Blood 120, no. 8 (2012): 1601–12. http://dx.doi.org/10.1182/blood-2011-11-393983.

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Abstract We recently defined a critical role for p53 in regulating the quiescence of adult hematopoietic stem cells (HSCs) and identified necdin as a candidate p53 target gene. Necdin is a growth-suppressing protein and the gene encoding it is one of several that are deleted in patients with Prader-Willi syndrome. To define the intrinsic role of necdin in adult hematopoiesis, in the present study, we transplanted necdin-null fetal liver cells into lethally irradiated recipients. We show that necdin-null adult HSCs are less quiescent and more proliferative than normal HSCs, demonstrating the si

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Singh, Shweta, Tanmoy Sarkar, Holly Morris, Kristbjorn Gudmundsson, and Jonathan Keller. "Id1 Ablation Rescues Clonal Hematopoiesis and Delays Disease Progression in Tet2 Null Mice." Blood 142, Supplement 1 (2023): 2694. http://dx.doi.org/10.1182/blood-2023-186744.

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Hematopoietic malignancies are thought to emerge through the gradual acquisition of genetic mutations within hematopoietic stem and progenitor cells (HSPCs). Some mutations impart a selective proliferative/growth advantage to HSPCs, which expand over time and contribute to a substantial percentage of mature blood cells. This increased proliferation and expansion is termed clonal hematopoiesis (CH) and is a preleukemic phase that is associated with an increased risk of accumulating additional mutations and developing leukemia. These mutations are also associated with increased inflammatory stre

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