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  1. Article ; Online: Parasite hijacks red cell membrane proteins.

    Mohandas, Narla / Blanc, Lionel

    Blood

    2023  Volume 142, Issue 23, Page(s) 1942–1944

    MeSH term(s) Animals ; Plasmodium falciparum ; Membrane Proteins ; Parasites ; Erythrocyte Membrane ; Erythrocytes
    Chemical Substances Membrane Proteins
    Language English
    Publishing date 2023-12-05
    Publishing country United States
    Document type Editorial ; Comment
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood.2023022781
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Blood cells molecules and diseases in 2022: A fountain of youth.

    Blanc, Lionel / Renella, Raffaele

    Blood cells, molecules & diseases

    2022  Volume 95, Page(s) 102665

    MeSH term(s) Adolescent ; Blood Cells ; Humans
    Language English
    Publishing date 2022-04-14
    Publishing country United States
    Document type Editorial
    ZDB-ID 1237083-6
    ISSN 1096-0961 ; 1079-9796
    ISSN (online) 1096-0961
    ISSN 1079-9796
    DOI 10.1016/j.bcmd.2022.102665
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  3. Article ; Online: Defending the island against excess heme.

    Blanc, Lionel / Lipton, Jeffrey M

    Blood

    2022  Volume 139, Issue 23, Page(s) 3359–3360

    MeSH term(s) Animals ; Erythroid Cells ; Erythropoiesis ; Heme ; Humans ; Mice ; Mice, Inbred DBA
    Chemical Substances Heme (42VZT0U6YR)
    Language English
    Publishing date 2022-06-09
    Publishing country United States
    Document type Editorial ; Comment
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood.2022016341
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  4. Article ; Online: Crosstalk between terminal erythropoiesis and granulopoiesis within their common niche: the erythromyeloblastic island.

    Romano, Laurel / Seu, Katie G / Blanc, Lionel / Kalfa, Theodosia A

    Current opinion in hematology

    2023  Volume 30, Issue 4, Page(s) 99–105

    Abstract: Purpose of review: The identity of the erythroblastic island (EBI) macrophage (Mϕ) has been under investigation for decades since it was recognized as the first hematopoietic niche 'nursing' terminal erythropoiesis. This review will focus on the current ...

    Abstract Purpose of review: The identity of the erythroblastic island (EBI) macrophage (Mϕ) has been under investigation for decades since it was recognized as the first hematopoietic niche 'nursing' terminal erythropoiesis. This review will focus on the current insights to the characteristics and the role of the EBI Mϕ balancing terminal erythropoiesis and granulopoiesis.
    Recent findings: While the EBI has long been known as the niche for erythroid precursors, significant advancements in biology research technologies, including optimization of EBI enrichment protocols, single-cell ribonucleic acid sequencing, and imaging flow cytometry, have recently revealed that granulocytic precursors co-exist in this niche, termed erythromyeloblastic island (EMBI). More importantly, the balance noted at baseline between terminal granulopoiesis and erythropoiesis within EBIs/EMBIs is altered with diseases affecting hematopoiesis, such as stress erythropoiesis and inflammatory conditions causing anemia of inflammation. The role of the EMBI niche has yet to be fully investigated mechanistically, however, a notable degree of transcriptional and cell surface marker heterogeneity has been identified for the EMBI Mϕ, implicating its plasticity and diverse function.
    Summary: Terminal erythropoiesis and granulopoiesis are regulated within the EMBI. Investigations of their balance within this niche in health and disease may reveal new targets for treatment of diseases of terminal hematopoiesis.
    MeSH term(s) Humans ; Erythropoiesis ; Erythroblasts/metabolism ; Anemia/metabolism ; Macrophages/metabolism ; Inflammation/metabolism
    Language English
    Publishing date 2023-04-25
    Publishing country United States
    Document type Review ; Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1153887-9
    ISSN 1531-7048 ; 1065-6251
    ISSN (online) 1531-7048
    ISSN 1065-6251
    DOI 10.1097/MOH.0000000000000767
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 3703: Show issues Location:
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  5. Article ; Online: Navigating the marrow sea towards erythromyeloblastic islands under normal and inflammatory conditions.

    Josselsohn, Rachel / Barnes, Betsy J / Kalfa, Theodosia A / Blanc, Lionel

    Current opinion in hematology

    2023  Volume 30, Issue 3, Page(s) 80–85

    Abstract: Purpose of review: Terminal erythroid differentiation occurs in specialized niches called erythroblastic islands. Since their discovery in 1958, these niches have been described as a central macrophage surrounded by differentiating erythroblasts. Here, ... ...

    Abstract Purpose of review: Terminal erythroid differentiation occurs in specialized niches called erythroblastic islands. Since their discovery in 1958, these niches have been described as a central macrophage surrounded by differentiating erythroblasts. Here, we review the recent advances made in the characterization of these islands and the role they could play in anaemia of inflammation.
    Recent findings: The utilization of multispectral imaging flow cytometry (flow cytometry with microscopy) has enabled for a more precise characterization of the niche that revealed the presence of maturing granulocytes in close contact with the central macrophage. These erythromyeloblastic islands (EMBIs) can adapt depending on the peripheral needs. Indeed, during inflammation wherein inflammatory cytokines limit erythropoiesis and promote granulopoiesis, EMBIs present altered structures with increased maturing granulocytes and decreased erythroid precursors.
    Summary: Regulation of the structure and function of the EMBI in the bone marrow emerges as a potential player in the pathophysiology of acute and chronic inflammation and its associated anaemia.
    MeSH term(s) Humans ; Bone Marrow/physiology ; Erythroblasts ; Erythropoiesis/physiology ; Anemia/etiology ; Inflammation
    Language English
    Publishing date 2023-01-17
    Publishing country United States
    Document type Review ; Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1153887-9
    ISSN 1531-7048 ; 1065-6251
    ISSN (online) 1531-7048
    ISSN 1065-6251
    DOI 10.1097/MOH.0000000000000756
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Is the erythropoietin receptor the key to the identification of the central macrophage in erythroblastic islands?

    Blanc, Lionel / Mohandas, Narla

    Blood science (Baltimore, Md.)

    2020  Volume 2, Issue 1, Page(s) 38–39

    Language English
    Publishing date 2020-01-16
    Publishing country United States
    Document type Journal Article
    ISSN 2543-6368
    ISSN (online) 2543-6368
    DOI 10.1097/BS9.0000000000000010
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  7. Article ; Online: Targeting of Calbindin 1 rescues erythropoiesis in a human model of Diamond Blackfan anemia.

    Wang, Nan / LaVasseur, Corinne / Riaz, Rao / Papoin, Julien / Blanc, Lionel / Narla, Anupama

    Blood cells, molecules & diseases

    2023  Volume 102, Page(s) 102759

    Abstract: Diamond Blackfan anemia (DBA) is an inherited bone marrow failure syndrome characterized by congenital anomalies, cancer predisposition and a severe hypo-proliferative anemia. It was the first disease linked to ribosomal dysfunction and >70 % of patients ...

    Abstract Diamond Blackfan anemia (DBA) is an inherited bone marrow failure syndrome characterized by congenital anomalies, cancer predisposition and a severe hypo-proliferative anemia. It was the first disease linked to ribosomal dysfunction and >70 % of patients have been identified to have a haploinsufficiency of a ribosomal protein (RP) gene, with RPS19 being the most common mutation. There is significant variability within the disease in terms of phenotype as well as response to therapy suggesting that other genes contribute to the pathophysiology and potential management of this disease. To explore these questions, we performed a genome-wide CRISPR screen in a cellular model of DBA and identified Calbindin 1 (CALB1), a member of the calcium-binding superfamily, as a potential modifier of the disordered erythropoiesis in DBA. We used human derived CD34+ cells cultured in erythroid stimulating media with knockdown of RPS19 as a model for DBA to study the effects of CALB1. We found that knockdown of CALB1 in this DBA model promoted erythroid maturation. We also noted effects of CALB1 knockdown on cell cycle. Taken together, our results reveal CALB1 is a novel regulator of human erythropoiesis and has implications for using CALB1 as a novel therapeutic target in DBA.
    MeSH term(s) Humans ; Anemia, Diamond-Blackfan/genetics ; Anemia, Diamond-Blackfan/therapy ; Erythropoiesis/genetics ; Calbindin 1/genetics ; Anemia ; Mutation
    Chemical Substances Calbindin 1
    Language English
    Publishing date 2023-05-26
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1237083-6
    ISSN 1096-0961 ; 1079-9796
    ISSN (online) 1096-0961
    ISSN 1079-9796
    DOI 10.1016/j.bcmd.2023.102759
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    Zs.A 1138: Show issues Location:
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  8. Article ; Online: Defects in Bone and Bone Marrow in Inherited Anemias: the Chicken or the Egg.

    Willimann, Rachel / Chougar, Christina / Wolfe, Lawrence C / Blanc, Lionel / Lipton, Jeffrey M

    Current osteoporosis reports

    2023  Volume 21, Issue 5, Page(s) 527–539

    Abstract: Purpose of review: Recently, there has been an increasing number of studies on the crosstalk between the bone and the bone marrow and how it pertains to anemia. Here, we discuss four heritable clinical syndromes contrasting those in which anemia affects ...

    Abstract Purpose of review: Recently, there has been an increasing number of studies on the crosstalk between the bone and the bone marrow and how it pertains to anemia. Here, we discuss four heritable clinical syndromes contrasting those in which anemia affects bone growth and development, with those in which abnormal bone development results in anemia, highlighting the multifaceted interactions between skeletal development and hematopoiesis.
    Recent findings: Anemia results from both inherited and acquired disorders caused by either impaired production or premature destruction of red blood cells or blood loss. The downstream effects on bone development and growth in patients with anemia often constitute an important part of their clinical condition. We will discuss the interdependence of abnormal bone development and growth and hematopoietic abnormalities, with a focus on the erythroid lineage. To illustrate those points, we selected four heritable anemias that arise from either defective hematopoiesis impacting the skeletal system (the hemoglobinopathies β-thalassemia and sickle cell disease) versus defective osteogenesis resulting in impaired hematopoiesis (osteopetrosis). Finally, we will discuss recent findings in Diamond Blackfan anemia, an intrinsic disorder of both the erythron and the bone. By focusing on four representative hereditary hematopoietic disorders, this complex relationship between bone and blood should lead to new areas of research in the field.
    MeSH term(s) Humans ; Bone Marrow ; Anemia/genetics ; Hematopoiesis/genetics ; Bone and Bones
    Language English
    Publishing date 2023-07-12
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 2186581-4
    ISSN 1544-2241 ; 1544-1873
    ISSN (online) 1544-2241
    ISSN 1544-1873
    DOI 10.1007/s11914-023-00809-3
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  9. Article ; Online: Stress erythropoiesis: selenium to the rescue!

    Dulmovits, Brian M / Blanc, Lionel

    Blood

    2018  Volume 131, Issue 23, Page(s) 2512–2513

    MeSH term(s) Erythropoiesis ; Selenium ; Selenoproteins ; Spleen
    Chemical Substances Selenoproteins ; Selenium (H6241UJ22B)
    Language English
    Publishing date 2018-06-07
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood-2018-04-844720
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  10. Article: CDK6-mediated endothelial cell cycle acceleration drives arteriovenous malformations in hereditary hemorrhagic telangiectasia.

    Dinakaran, Sajeth / Zhao, Haitian / Tang, Yuefeng / Wang, Zhimin / Ruiz, Santiago / Nomura-Kitabayashi, Aya / Blanc, Lionel / Faughnan, Marie E / Marambaud, Philippe

    bioRxiv : the preprint server for biology

    2023  

    Abstract: Increased endothelial cell (EC) proliferation is a hallmark of arteriovenous malformations (AVMs) in hereditary hemorrhagic telangiectasia (HHT). The underlying mechanism and disease relevance of this abnormal cell proliferative state of the ECs remain ... ...

    Abstract Increased endothelial cell (EC) proliferation is a hallmark of arteriovenous malformations (AVMs) in hereditary hemorrhagic telangiectasia (HHT). The underlying mechanism and disease relevance of this abnormal cell proliferative state of the ECs remain unknown. Here, we report the identification of a CDK6-driven mechanism of cell cycle progression deregulation directly involved in EC proliferation and HHT vascular pathology. Specifically, HHT mouse liver ECs exhibited defects in their cell cycle control characterized by a G1/S checkpoint bypass and acceleration of cell cycle speed. Phosphorylated retinoblastoma (p-RB1)-a marker of G1/S transition through the restriction point-significantly accumulated in ECs of HHT mouse retinal AVMs and HHT patient skin telangiectasias. Mechanistically, ALK1 loss of function increased the expression of key restriction point mediators, and treatment with palbociclib or ribociclib, two CDK4/6 inhibitors, blocked p-RB1 increase and retinal AVMs in HHT mice. Palbociclib also improved vascular pathology in the brain and slowed down endothelial cell cycle speed and EC proliferation. Specific deletion of
    Language English
    Publishing date 2023-09-16
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.09.15.554413
    Database MEDical Literature Analysis and Retrieval System OnLINE

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