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Article: Global transcriptome analysis of T-competent progenitors in the bone marrow

Yu, Vionnie W.C / Scadden, David T

Genomics Data. 2015 Sept., v. 5

2015

Abstract: ... cell immunity by regulating T progenitor development in the bone marrow (Yu et al., 2015) [1]. Selective ...

Abstract	T cells are known to develop in the thymus. However, molecular events that control the transition from hematopoietic progenitor cells in the bone marrow to T precursor cells seeded in the thymus remained poorly defined. Our recent report showed that osteocalcin (Ocn)-expressing bone cells in the bone marrow have major impact on T cell immunity by regulating T progenitor development in the bone marrow (Yu et al., 2015) [1]. Selective endogenous depletion of Ocn+cells by inducible diphtheria toxin receptor expression (OcnCre;iDTR) led to reduction of T-competent common lymphoid progenitors (Ly6D− CLPs) in the bone marrow and loss of T cells in the thymus. Expression of the Notch ligand DLL4 by Ocn+cells in the bone marrow ensures the production of Ly6D− CLPs, and expression of chemotactic molecules CCR7 and PSGL1 to enable subsequent thymic seeding. These data indicate that specific mesenchymal cells in bone marrow provide key molecular drivers enforcing thymus-seeding progenitor generation and thereby directly link skeletal biology to the production of T cell based adaptive immunity. Here we present the transcriptome profiles of Ly6D− CLPs derived from Ocn+ cells deleted mice (OcnCre+;iDTR) compared to those derived from control littermates (OcnCre−;iDTR). These data are publically available from NCBI Gene Expression Omnibus (GEO) with the accession number GSE66102.
Keywords	CCR7 receptor ; T-lymphocytes ; adaptive immunity ; bone marrow ; chemotaxis ; gene expression ; hematopoietic stem cells ; ligands ; mice ; osteocalcin ; sowing ; thymus gland ; transcriptomics
Language	English
Dates of publication	2015-09
Size	p. 100-102.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	2751131-5
ISSN	2213-5960
ISSN	2213-5960
DOI	10.1016/j.gdata.2015.05.024
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Heterogeneity of the bone marrow niche.

Yu, Vionnie W C / Scadden, David T

Current opinion in hematology

2016 Volume 23, Issue 4, Page(s) 331–338

Abstract: Purpose of review: The bone marrow niche is increasingly recognized as heterogeneous with specific subtypes of mesenchymal niche cells governing the development or homeostasis of selective parenchymal hematopoietic subsets. The present review outlines ... ...

Abstract	Purpose of review: The bone marrow niche is increasingly recognized as heterogeneous with specific subtypes of mesenchymal niche cells governing the development or homeostasis of selective parenchymal hematopoietic subsets. The present review outlines recent efforts in dissecting these microniches regulated by unique cell pairings within the bone marrow and provides an overview of how the bone marrow orchestrates multiple facets of hematopoiesis. Recent findings: Recent advancement in technologies has significantly improved our understanding of the cellular and molecular constituents that contribute to regulation of hematopoiesis and to maintenance of the hematopoietic stem cells (HSCs). Transgenic mouse models that enable endogenous cell deletion or lineage tracing, coupled with advanced intravital microscopy has identified several mesenchymal cell types, including the osteolineage cells, megakaryocytes, macrophages, perivascular cells, and Schwann cells, to be indispensible regulators of hematopoiesis. These niche cells, when perturbed, each caused very specific hematopoietic consequences including impairment in B-cell maturation, T lineage development, erythropoiesis, and impact different aspects of HSC behavior such as quiescence, mobilization, and response to acute stress signals. Summary: The emerging concept is that the bone marrow environment is composed of multiple microniches, each consisting of unique pairing of distinct supportive stromal cells with distinct hematopoietic subtypes to regulate a particular branch of hematopoietic cell process. The bone marrow can be viewed as a carrier with subcompartments tailored to support different hematopoietic activities.
MeSH term(s)	Animals ; Bone Marrow Cells/cytology ; Bone Marrow Cells/metabolism ; Cell Communication ; Cell Cycle ; Cell Differentiation ; Cell Movement ; Erythropoiesis ; Hematopoiesis ; Hematopoietic Stem Cells/cytology ; Hematopoietic Stem Cells/metabolism ; Humans ; Lymphoid Progenitor Cells/cytology ; Lymphoid Progenitor Cells/metabolism ; Lymphopoiesis ; Macrophages/metabolism ; Megakaryocytes/metabolism ; Mesenchymal Stem Cells/cytology ; Mesenchymal Stem Cells/metabolism ; Osteogenesis ; Stem Cell Niche ; Stress, Physiological ; Sympathetic Nervous System/physiology
Language	English
Publishing date	2016-03-17
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1153887-9
ISSN	1531-7048 ; 1065-6251
ISSN (online)	1531-7048
ISSN	1065-6251
DOI	10.1097/MOH.0000000000000265
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Article ; Online: CRISPR-Cas9 Editing of the

The New England journal of medicine

2023 Volume 389, Issue 9, Page(s) 820–832

Abstract: Background: Sickle cell disease is caused by a defect in the β-globin subunit of adult hemoglobin. Sickle hemoglobin polymerizes under hypoxic conditions, producing deformed red cells that hemolyze and cause vaso-occlusion that results in progressive ... ...

Abstract	Background: Sickle cell disease is caused by a defect in the β-globin subunit of adult hemoglobin. Sickle hemoglobin polymerizes under hypoxic conditions, producing deformed red cells that hemolyze and cause vaso-occlusion that results in progressive organ damage and early death. Elevated fetal hemoglobin levels in red cells protect against complications of sickle cell disease. OTQ923, a clustered regularly interspaced short palindromic repeats (CRISPR)-Cas9-edited CD34+ hematopoietic stem- and progenitor-cell (HSPC) product, has a targeted disruption of the Methods: We performed a tiling CRISPR-Cas9 screen of the Results: In preclinical experiments, CD34+ HSPCs (obtained from healthy donors and persons with sickle cell disease) edited with CRISPR-Cas9 and gRNA-68 had sustained on-target editing with no off-target mutations and produced high levels of fetal hemoglobin after in vitro differentiation or xenotransplantation into immunodeficient mice. In the study, three participants received autologous OTQ923 after myeloablative conditioning and were followed for 6 to 18 months. At the end of the follow-up period, all the participants had engraftment and stable induction of fetal hemoglobin (fetal hemoglobin as a percentage of total hemoglobin, 19.0 to 26.8%), with fetal hemoglobin broadly distributed in red cells (F cells as a percentage of red cells, 69.7 to 87.8%). Manifestations of sickle cell disease decreased during the follow-up period. Conclusions: CRISPR-Cas9 disruption of the
MeSH term(s)	Animals ; Mice ; Anemia, Sickle Cell/genetics ; Anemia, Sickle Cell/therapy ; Antigens, CD34 ; CRISPR-Cas Systems ; Erythrocytes ; Fetal Hemoglobin/biosynthesis ; Fetal Hemoglobin/genetics ; Fetal Hemoglobin/metabolism ; Hemoglobin, Sickle ; Promoter Regions, Genetic ; Hematopoietic Stem Cell Transplantation
Chemical Substances	Antigens, CD34 ; Fetal Hemoglobin (9034-63-3) ; Hemoglobin, Sickle
Language	English
Publishing date	2023-08-30
Publishing country	United States
Document type	Clinical Trial, Phase I ; Clinical Trial, Phase II ; Journal Article ; Multicenter Study
ZDB-ID	207154-x
ISSN	1533-4406 ; 0028-4793
ISSN (online)	1533-4406
ISSN	0028-4793
DOI	10.1056/NEJMoa2215643
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Article: Global transcriptome analysis of T-competent progenitors in the bone marrow.

Yu, Vionnie W C / Scadden, David T

Genomics data

2015 Volume 5, Page(s) 100–102

Abstract: ... cell immunity by regulating T progenitor development in the bone marrow (Yu et al., 2015) [1]. Selective ...

Abstract	T cells are known to develop in the thymus. However, molecular events that control the transition from hematopoietic progenitor cells in the bone marrow to T precursor cells seeded in the thymus remained poorly defined. Our recent report showed that osteocalcin (Ocn)-expressing bone cells in the bone marrow have major impact on T cell immunity by regulating T progenitor development in the bone marrow (Yu et al., 2015) [1]. Selective endogenous depletion of Ocn(+) cells by inducible diphtheria toxin receptor expression (OcnCre;iDTR) led to reduction of T-competent common lymphoid progenitors (Ly6D(-) CLPs) in the bone marrow and loss of T cells in the thymus. Expression of the Notch ligand DLL4 by Ocn(+) cells in the bone marrow ensures the production of Ly6D(-) CLPs, and expression of chemotactic molecules CCR7 and PSGL1 to enable subsequent thymic seeding. These data indicate that specific mesenchymal cells in bone marrow provide key molecular drivers enforcing thymus-seeding progenitor generation and thereby directly link skeletal biology to the production of T cell based adaptive immunity. Here we present the transcriptome profiles of Ly6D(-) CLPs derived from Ocn(+) cells deleted mice (OcnCre(+);iDTR) compared to those derived from control littermates (OcnCre(-);iDTR). These data are publically available from NCBI Gene Expression Omnibus (GEO) with the accession number GSE66102.
Language	English
Publishing date	2015-06-05
Publishing country	United States
Document type	Journal Article
ZDB-ID	2751131-5
ISSN	2213-5960
ISSN	2213-5960
DOI	10.1016/j.gdata.2015.05.024
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Article: Transcriptome comparison of distinct osteolineage subsets in the hematopoietic stem cell niche using a triple fluorescent transgenic mouse model

Yu, Vionnie W.C / Lymperi, Stefania / Ferraro, Francesca / Scadden, David T

Genomics Data. 2015 Sept., v. 5

2015

Abstract: ... deletion of osteocalcin-expressing (Ocn+) cells led to a loss of T immune cells (Yu et al., 2015 [8]. Ocn+ ...

Abstract	The bone marrow niche is recognized as a central player in maintaining and regulating the behavior of hematopoietic stem and progenitor cells. Specific gain-of and loss-of function experiments perturbing a range of osteolineage cells or their secreted proteins had been shown to affect stem cell maintenance (Calvi et al, 2003 [1]; Stier et al., 2005 [2]; Zhang et al., 2003 [3]; Nilsson et al., 2005 [4]; Greenbaum et al., 2013 [5]) and engraftment (Adam et al., 2006, 2009 [6,7]). We used specific in vivo cell deletion approaches to dissect the niche cell-parenchymal cell dependency in a complex bone marrow microenvironment. Endogenous deletion of osteocalcin-expressing (Ocn+) cells led to a loss of T immune cells (Yu et al., 2015 [8]. Ocn+ cells express the Notch ligand DLL4 to communicate with T-competent progenitors, and thereby ensuring T precursor production and expression of chemotactic molecules on their cell surface for subsequent thymic seeding. In contrast, depletion of osterix-expressing (Osx+) osteoprogenitors led to reduced B immune cells. These distinct hematopoietic phenotypes suggest specific pairing of mesenchymal niche cells and parenchymal hematopoietic cells in the bone marrow to create unique functional units to support hematopoiesis. Here, we present the global gene expression profiles of these osteolineage subtypes utilizing a triple fluorescent transgenic mouse model (OsxCre+;Rosa-mCh+;Ocn:Topaz+) that labels Osx+ cells red, Ocn+ cells green, and Osx+Ocn+ cells yellow. This system allows isolation of distinct osteolineage subsets within the same animal by flow cytometry. Array data that have been described in our study [8] are also publically available from NCBI Gene Expression Omnibus (GEO) with the accession number GSE66042. Differences in gene expression may correlate with functional difference in supporting hematopoiesis.
Keywords	animal models ; bone marrow ; chemotaxis ; flow cytometry ; fluorescence ; gene expression ; hematopoiesis ; hematopoietic stem cells ; ligands ; phenotype ; protein secretion ; sowing ; transcriptome ; transgenic animals
Language	English
Dates of publication	2015-09
Size	p. 318-319.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	2751131-5
ISSN	2213-5960
ISSN	2213-5960
DOI	10.1016/j.gdata.2015.06.001
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Article: Transcriptome comparison of distinct osteolineage subsets in the hematopoietic stem cell niche using a triple fluorescent transgenic mouse model.

Yu, Vionnie W C / Lymperi, Stefania / Ferraro, Francesca / Scadden, David T

Genomics data

2015 Volume 5, Page(s) 318–319

Abstract: ... deletion of osteocalcin-expressing (Ocn(+)) cells led to a loss of T immune cells (Yu et al., 2015 [8]. Ocn ...

Abstract	The bone marrow niche is recognized as a central player in maintaining and regulating the behavior of hematopoietic stem and progenitor cells. Specific gain-of and loss-of function experiments perturbing a range of osteolineage cells or their secreted proteins had been shown to affect stem cell maintenance (Calvi et al, 2003 [1]; Stier et al., 2005 [2]; Zhang et al., 2003 [3]; Nilsson et al., 2005 [4]; Greenbaum et al., 2013 [5]) and engraftment (Adam et al., 2006, 2009 [6,7]). We used specific in vivo cell deletion approaches to dissect the niche cell-parenchymal cell dependency in a complex bone marrow microenvironment. Endogenous deletion of osteocalcin-expressing (Ocn(+)) cells led to a loss of T immune cells (Yu et al., 2015 [8]. Ocn(+) cells express the Notch ligand DLL4 to communicate with T-competent progenitors, and thereby ensuring T precursor production and expression of chemotactic molecules on their cell surface for subsequent thymic seeding. In contrast, depletion of osterix-expressing (Osx(+)) osteoprogenitors led to reduced B immune cells. These distinct hematopoietic phenotypes suggest specific pairing of mesenchymal niche cells and parenchymal hematopoietic cells in the bone marrow to create unique functional units to support hematopoiesis. Here, we present the global gene expression profiles of these osteolineage subtypes utilizing a triple fluorescent transgenic mouse model (OsxCre(+);Rosa-mCh(+);Ocn:Topaz(+)) that labels Osx(+) cells red, Ocn(+) cells green, and Osx(+) Ocn(+) cells yellow. This system allows isolation of distinct osteolineage subsets within the same animal by flow cytometry. Array data that have been described in our study [8] are also publically available from NCBI Gene Expression Omnibus (GEO) with the accession number GSE66042. Differences in gene expression may correlate with functional difference in supporting hematopoiesis.
Language	English
Publishing date	2015-06-05
Publishing country	United States
Document type	Journal Article
ZDB-ID	2751131-5
ISSN	2213-5960
ISSN	2213-5960
DOI	10.1016/j.gdata.2015.06.001
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Distinctive Mesenchymal-Parenchymal Cell Pairings Govern B Cell Differentiation in the Bone Marrow

Vionnie W.C. Yu / Stefania Lymperi / Toshihiko Oki / Alexandra Jones / Peter Swiatek / Radovan Vasic / Francesca Ferraro / David T. Scadden

Stem Cell Reports, Vol 7, Iss 2, Pp 220-

2016 Volume 235

Abstract: Bone marrow niches for hematopoietic progenitor cells are not well defined despite their critical role in blood homeostasis. We previously found that cells expressing osteocalcin, a marker of mature osteolineage cells, regulate the production of thymic- ... ...

Abstract	Bone marrow niches for hematopoietic progenitor cells are not well defined despite their critical role in blood homeostasis. We previously found that cells expressing osteocalcin, a marker of mature osteolineage cells, regulate the production of thymic-seeding T lymphoid progenitors. Here, using a selective cell deletion strategy, we demonstrate that a subset of mesenchymal cells expressing osterix, a marker of bone precursors in the adult, serve to regulate the maturation of early B lymphoid precursors by promoting pro-B to pre-B cell transition through insulin-like growth factor 1 (IGF-1) production. Loss of Osx+ cells or Osx-specific deletion of IGF-1 led to a failure of B cell maturation and the impaired adaptive immune response. These data highlight the notion that bone marrow is a composite of specialized niches formed by pairings of specific mesenchymal cells with parenchymal stem or lineage committed progenitor cells, thereby providing distinctive functional units to regulate hematopoiesis.
Keywords	Medicine (General) ; R5-920 ; Biology (General) ; QH301-705.5
Language	English
Publishing date	2016-08-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Epigenetic Memory Underlies Cell-Autonomous Heterogeneous Behavior of Hematopoietic Stem Cells.

Yu, Vionnie W C / Yusuf, Rushdia Z / Oki, Toshihiko / Wu, Juwell / Saez, Borja / Wang, Xin / Cook, Colleen / Baryawno, Ninib / Ziller, Michael J / Lee, Eunjung / Gu, Hongcang / Meissner, Alexander / Lin, Charles P / Kharchenko, Peter V / Scadden, David T

Cell

2017 Volume 168, Issue 5, Page(s) 944–945

Language	English
Publishing date	2017-02-13
Publishing country	United States
Document type	Journal Article ; Published Erratum
ZDB-ID	187009-9
ISSN	1097-4172 ; 0092-8674
ISSN (online)	1097-4172
ISSN	0092-8674
DOI	10.1016/j.cell.2017.02.010
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Article ; Online: FIAT Deletion Increases Bone Mass But Does Not Prevent High-Fat-Diet-Induced Metabolic Complications.

Hekmatnejad, Bahareh / Yu, Vionnie W C / Addison, William / Mandic, Vice / Pellicelli, Martin / Arabian, Alice / St-Arnaud, René

Endocrinology

2017 Volume 158, Issue 2, Page(s) 264–276

Abstract: Factor inhibiting activating transcription factor 4 (ATF4)-mediated transcription (FIAT) interacts with ATF4 to repress its transcriptional activity. We performed a phenotypic analysis of Fiat-deficient male mice (Fiat-/Y) at 8 and 16 weeks of age. ... ...

Abstract	Factor inhibiting activating transcription factor 4 (ATF4)-mediated transcription (FIAT) interacts with ATF4 to repress its transcriptional activity. We performed a phenotypic analysis of Fiat-deficient male mice (Fiat-/Y) at 8 and 16 weeks of age. Microcomputed tomography analysis of the distal femur demonstrated 46% and 13% age-dependent increases in trabecular bone volume and thickness, respectively, in Fiat-/Y mice. Cortical bone measurements at the femoral midshaft revealed a substantial increase in cortical thickness in older Fiat-/Y mice. Bone gain was related to increased mineral apposition rate and increased osteoblast function. Femoral stiffness and strength were substantially increased in Fiat-/Y compared with wild-type (WT) mice. We also investigated whether FIAT contributes to metabolic function. When fed standard mouse chow, Fiat-/Y animals were glucose-tolerant. However, when fed a high-fat diet (HFD) for 8 weeks, Fiat-/Y mice gained more weight than control mice, with a specific increase in white adipose tissue fat mass. The increase in fat mass was due to reduced energy expenditure, which correlated with reduced fatty acid oxidation and lipolysis in the adipose tissue of mutant mice. The expression of the Scd1 gene, involved in lipogenesis, was upregulated in the subcutaneous adipose tissue of Fiat-/Y mice. Moreover, HFD-fed Fiat-/Y mice exhibited increased circulating leptin and insulin levels relative to WT mice, demonstrating that endocrine abnormalities are associated with the disturbance in energy balance. We conclude that Fiat-/Y mice exhibited an anabolic bone phenotype but displayed increased susceptibility to developing metabolic-related disorders when consuming an HFD.
MeSH term(s)	Adipose Tissue, White/metabolism ; Adiposity ; Age Factors ; Animals ; Body Weight ; Bone Density ; Co-Repressor Proteins/genetics ; Co-Repressor Proteins/metabolism ; Diet, High-Fat/adverse effects ; Energy Metabolism ; Lipogenesis ; Lipolysis ; Mice, Knockout ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; Osteoblasts/metabolism ; Oxygen Consumption ; Phenotype ; Weight-Bearing
Chemical Substances	Co-Repressor Proteins ; Nuclear Proteins ; Txkng protein, mouse
Language	English
Publishing date	2017--01
Publishing country	United States
Document type	Journal Article
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/en.2016-1867
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Article ; Online: Distinctive Mesenchymal-Parenchymal Cell Pairings Govern B Cell Differentiation in the Bone Marrow.

Yu, Vionnie W C / Lymperi, Stefania / Oki, Toshihiko / Jones, Alexandra / Swiatek, Peter / Vasic, Radovan / Ferraro, Francesca / Scadden, David T

Stem cell reports

2016 Volume 7, Issue 2, Page(s) 220–235

Abstract	Bone marrow niches for hematopoietic progenitor cells are not well defined despite their critical role in blood homeostasis. We previously found that cells expressing osteocalcin, a marker of mature osteolineage cells, regulate the production of thymic-seeding T lymphoid progenitors. Here, using a selective cell deletion strategy, we demonstrate that a subset of mesenchymal cells expressing osterix, a marker of bone precursors in the adult, serve to regulate the maturation of early B lymphoid precursors by promoting pro-B to pre-B cell transition through insulin-like growth factor 1 (IGF-1) production. Loss of Osx(+) cells or Osx-specific deletion of IGF-1 led to a failure of B cell maturation and the impaired adaptive immune response. These data highlight the notion that bone marrow is a composite of specialized niches formed by pairings of specific mesenchymal cells with parenchymal stem or lineage committed progenitor cells, thereby providing distinctive functional units to regulate hematopoiesis.
Language	English
Publishing date	2016-08-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	2720528-9
ISSN	2213-6711 ; 2213-6711
ISSN (online)	2213-6711
ISSN	2213-6711
DOI	10.1016/j.stemcr.2016.06.009
Database	MEDical Literature Analysis and Retrieval System OnLINE

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