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Article: [GATA factor-related hematopoietic diseases].

Shimizu, Ritsuko

Rinsho ketsueki] The Japanese journal of clinical hematology

2020 Volume 61, Issue 9, Page(s) 1112–1119

Abstract: GATA1-deficient mice die in utero on 12.5 embryonic day (E12.5) due to a complete block of primitive erythropoiesis in the yolk sac, while GATA2-deficient mice die on E10.5 due to severe anemia and hemorrhage, since GATA2 is essential for the development ...

Abstract	GATA1-deficient mice die in utero on 12.5 embryonic day (E12.5) due to a complete block of primitive erythropoiesis in the yolk sac, while GATA2-deficient mice die on E10.5 due to severe anemia and hemorrhage, since GATA2 is essential for the development of hemangioblasts, which are common precursor cells of hematopoietic stem cells and endothelial cells. In contrast, GATA3 is critical to the development of Th2 cells. However, GATA3-deficient mice die in utero before the particular phenotype of hematopoietic system emerges, which is caused by a defect in the development of nervous and renal urinary systems. It has been well elucidated that defects in the hematopoietic GATA factors disturb hematopoietic homeostasis. However, details on how GATA factor dysfunction leads to human hematopoietic diseases remain to be clarified. At the end of the twentieth century, several mutations in GATA1 gene were identified as the cause of familial thrombocytopenia. Since then, various types of hematopoietic diseases elicited by GATA1 and GATA2 dysfunctions have been reported. This review summarizes recent topics of GATA factor-related hematopoietic diseases.
MeSH term(s)	Animals ; Endothelial Cells ; Erythropoiesis ; GATA Transcription Factors ; Hematologic Diseases ; Hematopoietic Stem Cells
Chemical Substances	GATA Transcription Factors
Language	Japanese
Publishing date	2020-11-25
Publishing country	Japan
Document type	Journal Article ; Review
ZDB-ID	390900-1
ISSN	0485-1439
ISSN	0485-1439
DOI	10.11406/rinketsu.61.1112
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Article: The abundance of the short GATA1 isoform affects megakaryocyte differentiation and leukemic predisposition in mice.

Ishihara, Daishi / Hasegawa, Atsushi / Hirano, Ikuo / Engel, James Douglas / Yamamoto, Masayuki / Shimizu, Ritsuko

Experimental hematology & oncology

2024 Volume 13, Issue 1, Page(s) 24

Abstract: Transcription factor GATA1 controls the delicate balance between proliferation, differentiation and apoptosis in both the erythroid and megakaryocytic lineages. In addition to full-length GATA1, there is an GATA1 isoform, GATA1s, that lacks the amino- ... ...

Abstract	Transcription factor GATA1 controls the delicate balance between proliferation, differentiation and apoptosis in both the erythroid and megakaryocytic lineages. In addition to full-length GATA1, there is an GATA1 isoform, GATA1s, that lacks the amino-terminal transactivation domain. Somatic GATA1 mutations that lead to the exclusive production of GATA1s appear to be necessary and sufficient for the development of a preleukemic condition called transient myeloproliferative disorder (TMD) in Down syndrome newborns. Subsequent clonal evolution among latent TMD blasts leads to the development of acute megakaryoblastic leukemia (AMKL). We originally established transgenic mice that express only GATA1s, which exhibit hyperproliferation of immature megakaryocytes, thus mimicking human TMD; however, these mice never developed AMKL. Here, we report that transgenic mice expressing moderate levels of GATA1s, i.e., roughly comparable levels to endogenous GATA1, were prone to develop AMKL in young adults. However, when GATA1s is expressed at levels significantly exceeding that of endogenous GATA1, the development of leukemia was restrained in a dose dependent manner. If the transgenic increase of GATA1s in progenitors remains small, GATA1s supports the terminal maturation of megakaryocyte progenitors insufficiently, and consequently the progenitors persisted, leading to an increased probability for acquisition of additional genetic modifications. In contrast, more abundant GATA1s expression compensates for this maturation block, enabling megakaryocytic progenitors to fully differentiate. This study provides evidence for the clinical observation that the abundance of GATA1s correlates well with the progression to AMKL in Down syndrome.
Language	English
Publishing date	2024-02-26
Publishing country	England
Document type	Letter
ZDB-ID	2669066-4
ISSN	2162-3619
ISSN	2162-3619
DOI	10.1186/s40164-024-00492-9
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Article: Strain-dependent modifiers exacerbate familial leukemia caused by GATA1-deficiency.

Hirano, Ikuo / Abe, Kanako / Engel, James Douglas / Yamamoto, Masayuki / Shimizu, Ritsuko

Experimental hematology & oncology

2024 Volume 13, Issue 1, Page(s) 23

Abstract: GATA1 plays a critical role in differentiation, proliferation, and apoptosis during erythropoiesis. We developed a Gata1 knock-down allele (Gata1.05) that results in GATA1 expression at 5% of endogenous level. In female mice heterozygous for both the ... ...

Abstract	GATA1 plays a critical role in differentiation, proliferation, and apoptosis during erythropoiesis. We developed a Gata1 knock-down allele (Gata1.05) that results in GATA1 expression at 5% of endogenous level. In female mice heterozygous for both the Gata1.05 and wild-type alleles, we observed a predisposition to erythroblastic leukemia three to six months after birth. Since no male Gata1.05 progeny survive gestation, we originally maintained heterozygous females in a mixed genetic background of C57BL/6J and DBA/2 strains. Around 30% of these mice reproducibly develop leukemia, but the other subset did not develop leukemia, even though they harbor a high number of preleukemic erythroblasts. These observations prompted us to hypothesize that there may be potential influence of genetic determinants on the progression of Gata1.05-driven hematopoietic precursors to full-blown leukemia. In an initial examination of Gata1.05/X mice backcrossed into C3H/He, BALB/c, DBA/2, C57BL/6J and 129X1/SvJ strains, we discerned that the backgrounds of C57BL/6J and 129X1/SvJ significantly expedited leukemia onset in Gata1.05/X mice. Conversely, backgrounds of C3H/He, BALB/c and DBA/2 did not substantially modify the effect of the Gata1 mutation. This indicates the existence of genetic modifiers that accentuate Gata1.05 leukemogenesis. Subsequent cohort studies evaluated Gata1.05/X mice within mix backgrounds of BALB/c:129X1/SvJ and BALB/c:C57BL/6J. In these settings, Gata1.05-driven leukemia manifested in autosomal dominant patterns within the 129X1/SvJ background and in autosomal recessive patterns within C57BL/6J background. To the best of our knowledge, this study provides the inaugural evidence of genetic modifiers that can reshape the outcome based on leukemia-associated gene signatures.
Language	English
Publishing date	2024-02-26
Publishing country	England
Document type	Letter
ZDB-ID	2669066-4
ISSN	2162-3619
ISSN	2162-3619
DOI	10.1186/s40164-024-00491-w
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Article ; Online: Intracanal microbiome profiles of two apical periodontitis cases in one patient: A comparison with saliva and plaque profiles.

Yamaki, Keiko / Tamahara, Toru / Washio, Jumpei / Sato, Takuichi / Shimizu, Ritsuko / Yamada, Satoru

Clinical and experimental dental research

2024 Volume 10, Issue 2, Page(s) e862

Abstract: Objectives: To determine the characteristics of the endodontic microbiome.: Material and methods: Saliva, plaque, and infected root canal wall dentin of two teeth suffering from apical periodontitis were harvested from a 58-year-old man. Bacterial ... ...

Abstract	Objectives: To determine the characteristics of the endodontic microbiome. Material and methods: Saliva, plaque, and infected root canal wall dentin of two teeth suffering from apical periodontitis were harvested from a 58-year-old man. Bacterial DNA was extracted from each sample, and 16S rRNA gene analysis targeting the V3-V4 region was conducted on the Illumina MiSeq platform using QIIME2. The functional potential of the microbiomes was inferred using PICRUSt2. Results: The four microbiomes were different in structure and membership, yet the nine most abundant metabolic pathways were common among them. The two endodontic microbiomes were more anaerobic, rich in Firmicutes, and scarce in Actinobacteriota and Proteobacteria, compared with saliva and plaque microbiomes. Their profiles were dissimilar despite their clinical and radiographic similarities. Conclusions: The endodontic microbiomes were anaerobic, rich in Firmicutes, scarce in Actinobacteriota and Proteobacteria, and considerably varied within an individual.
MeSH term(s)	Male ; Humans ; Middle Aged ; Saliva ; RNA, Ribosomal, 16S/genetics ; Dental Plaque ; Periapical Periodontitis ; Microbiota/genetics
Chemical Substances	RNA, Ribosomal, 16S
Language	English
Publishing date	2024-03-04
Publishing country	United States
Document type	Case Reports ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2829558-4
ISSN	2057-4347 ; 2057-4347
ISSN (online)	2057-4347
ISSN	2057-4347
DOI	10.1002/cre2.862
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Article ; Online: Quantitative and qualitative impairments in GATA2 and myeloid neoplasms.

Shimizu, Ritsuko / Yamamoto, Masayuki

IUBMB life

2019 Volume 72, Issue 1, Page(s) 142–150

Abstract: GATA2 is a key transcription factor critical for hematopoietic cell development. During the past decade, it became clear that heterozygous germline mutations in the GATA2 gene cause bone marrow failure and primary immunodeficiency syndrome, conditions ... ...

Abstract	GATA2 is a key transcription factor critical for hematopoietic cell development. During the past decade, it became clear that heterozygous germline mutations in the GATA2 gene cause bone marrow failure and primary immunodeficiency syndrome, conditions that lead to a predisposition toward myeloid neoplasms, such as myelodysplastic syndrome, acute myeloid leukemia, and chronic myelomonocytic leukemia. Somatic mutations of the GATA2 gene are also involved in the pathogenesis of myeloid malignancies. Cases with GATA2 gene mutations are divided into two groups, resulting in either a quantitative deficiency or a qualitative defect in the GATA2 protein depending on the mutation position and type. In the former case, GATA2 mRNA expression from the mutant allele is markedly reduced or completely abrogated, and reduced GATA2 protein expression is involved in the pathogenesis. In the latter case, almost equal amounts of structurally abnormal and wildtype GATA2 proteins are predicted to be present and contribute to the pathogenesis. The development of mouse models of these human GATA2-related diseases has been undertaken, which naturally develop myeloid neoplasms.
MeSH term(s)	Animals ; Cell Differentiation ; GATA2 Transcription Factor/genetics ; GATA2 Transcription Factor/metabolism ; Humans ; Mutation ; Myelodysplastic Syndromes/genetics ; Myelodysplastic Syndromes/pathology
Chemical Substances	GATA2 Transcription Factor
Language	English
Publishing date	2019-11-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1492141-8
ISSN	1521-6551 ; 1521-6543
ISSN (online)	1521-6551
ISSN	1521-6543
DOI	10.1002/iub.2188
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Article: [Leukemogenesis caused by dysfunctions of GATA1 transcription factor].

Shimizu, Ritsuko

Rinsho ketsueki] The Japanese journal of clinical hematology

2011 Volume 52, Issue 8, Page(s) 695–702

MeSH term(s)	Animals ; GATA1 Transcription Factor/genetics ; Gene Expression Regulation, Leukemic/genetics ; Humans ; Leukemia, Erythroblastic, Acute/genetics ; Leukemia, Megakaryoblastic, Acute/genetics ; Mice ; Mutation
Chemical Substances	GATA1 Transcription Factor ; GATA1 protein, human
Language	Japanese
Publishing date	2011-08
Publishing country	Japan
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	390900-1
ISSN	0485-1439
ISSN	0485-1439
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Article: GATA1 Activity Governed by Configurations of

Hasegawa, Atsushi / Shimizu, Ritsuko

Frontiers in oncology

2017 Volume 6, Page(s) 269

Abstract: The transcription factor GATA1 regulates the expression of essential erythroid and megakaryocytic differentiation genes through binding to the DNA consensus sequence WGATAR. The GATA1 protein has four functional domains, including two centrally located ... ...

Abstract	The transcription factor GATA1 regulates the expression of essential erythroid and megakaryocytic differentiation genes through binding to the DNA consensus sequence WGATAR. The GATA1 protein has four functional domains, including two centrally located zinc-finger domains and two transactivation domains at the N- and C-termini. These functional domains play characteristic roles in the elaborate regulation of diversified GATA1 target genes, each of which exhibits a unique expression profile. Three types of GATA1-related hematological malignancies have been reported. One is a structural mutation in the GATA1 gene, resulting in the production of a short form of GATA1 that lacks the N-terminal transactivation domain and is found in Down syndrome-related acute megakaryocytic leukemia. The other two are
Language	English
Publishing date	2017-01-09
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2649216-7
ISSN	2234-943X
ISSN	2234-943X
DOI	10.3389/fonc.2016.00269
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Article ; Online: The Significance of Bile in the Biliopancreatic Limb on Metabolic Improvement After Duodenal-Jejunal Bypass.

Kawana, Tomomi / Imoto, Hirofumi / Tanaka, Naoki / Tsuchiya, Takahiro / Yamamura, Akihiro / Saijo, Fumito / Maekawa, Masamitsu / Tamahara, Toru / Shimizu, Ritsuko / Nakagawa, Kei / Ohnuma, Shinobu / Kamei, Takashi / Unno, Michiaki

Obesity surgery

2024 Volume 34, Issue 5, Page(s) 1665–1673

Abstract: Introduction: Duodenal-jejunal bypass (DJB) is an experimental procedure in metabolic surgery that does not have a restrictive component. Changes in bile acid (BA) dynamics and intestinal microbiota are possibly related to metabolic improvement after ... ...

Abstract	Introduction: Duodenal-jejunal bypass (DJB) is an experimental procedure in metabolic surgery that does not have a restrictive component. Changes in bile acid (BA) dynamics and intestinal microbiota are possibly related to metabolic improvement after DJB. Our previous studies involving obese diabetic rats showed the crucial role of the biliopancreatic limb (BPL) in metabolic improvement after DJB caused by BA reabsorption. We established a new DJB procedure to prevent bile from flowing into the BPL and aimed to elucidate the importance of bile in the BPL after DJB. Methods: Otsuka Long-Evans Tokushima Fatty rats with diabetes were divided into three groups: two DJB groups and a sham group (n = 11). Duodenal-jejunal anastomosis was performed proximal to the papilla of Vater in the DJB group (n = 11). However, the DJB-D group (n = 11) underwent a new procedure with duodenal-jejunal anastomosis distal to the papilla of Vater for preventing bile flow into the BPL. Results: Glucose metabolism improved and weight gain was suppressed in the DJB group, but not in the DJB-D and sham groups. Serum BA level and conjugated BA concentration were elevated in the DJB group. The gut microbiota was altered only in the DJB group; the abundance of Firmicutes and Bacteroidetes decreased and that of Actinobacteria increased. However, the DJB-D group exhibited no apparent change in the gut microbiota, similar to the sham group. Conclusion: BAs are essential in the BPL for metabolic improvement after DJB; they can improve the gut microbiota in these processes.
MeSH term(s)	Rats ; Animals ; Bile ; Diabetes Mellitus, Experimental/surgery ; Diabetes Mellitus, Type 2/surgery ; Diabetes Mellitus, Type 2/metabolism ; Obesity, Morbid/surgery ; Jejunum/surgery ; Jejunum/metabolism ; Duodenum/surgery ; Duodenum/metabolism ; Bile Acids and Salts/metabolism ; Blood Glucose/metabolism ; Gastric Bypass/methods
Chemical Substances	Bile Acids and Salts ; Blood Glucose
Language	English
Publishing date	2024-03-21
Publishing country	United States
Document type	Journal Article
ZDB-ID	1070827-3
ISSN	1708-0428 ; 0960-8923
ISSN (online)	1708-0428
ISSN	0960-8923
DOI	10.1007/s11695-024-07176-7
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Article ; Online: GATA-related hematologic disorders.

Shimizu, Ritsuko / Yamamoto, Masayuki

Experimental hematology

2016 Volume 44, Issue 8, Page(s) 696–705

Abstract: The transcription factors GATA1 and GATA2 are fundamental regulators of hematopoiesis and have overlapping expression profiles. GATA2 is expressed in hematopoietic stem cells and early erythroid-megakaryocytic progenitors and activates a certain set of ... ...

Abstract	The transcription factors GATA1 and GATA2 are fundamental regulators of hematopoiesis and have overlapping expression profiles. GATA2 is expressed in hematopoietic stem cells and early erythroid-megakaryocytic progenitors and activates a certain set of early-phase genes, including the GATA2 gene itself. GATA2 also initiates GATA1 gene expression. In contrast, GATA1 is expressed in relatively mature erythroid progenitors and facilitates the expression of genes associated with differentiation, including the GATA1 gene itself; however, GATA1 represses the expression of GATA2. Switching the GATA factors from GATA2 to GATA1 appears to be one of the key regulatory mechanisms underlying erythroid differentiation. Loss-of-function analyses using mice in vivo have indicated that GATA2 and GATA1 are functionally nonredundant and that neither can compensate for the absence of the other. However, transgenic expression of GATA2 under the transcriptional regulation of the Gata1 gene rescues lethal dyserythropoiesis in GATA1-deficient mice, illustrating that the dynamic expression profiles of these GATA factors are critically important for the maintenance of hematopoietic homeostasis. Analysis of naturally occurring leukemias in GATA1-knockdown mice revealed that leukemic stem cells undergo functional alterations in response to exposure to chemotherapeutic agents. This mechanism may also underlie the aggravating features of relapsing leukemias. Recent hematologic analyses have suggested that disturbances in the balance of the GATA factors are associated with specific types of hematopoietic disorders. Here, we describe GATA1- and GATA2-related hematologic diseases, focusing on the regulation of GATA factor gene expression.
MeSH term(s)	Animals ; Cell Transformation, Neoplastic/genetics ; GATA Transcription Factors/genetics ; GATA Transcription Factors/metabolism ; GATA1 Transcription Factor/genetics ; GATA1 Transcription Factor/metabolism ; GATA2 Transcription Factor/genetics ; GATA2 Transcription Factor/metabolism ; Gene Expression Regulation ; Genetic Variation ; Haploinsufficiency ; Hematologic Diseases/etiology ; Hematologic Diseases/metabolism ; Humans ; Mutation ; Polymorphism, Genetic ; Protein Interaction Domains and Motifs ; Transcriptional Activation
Chemical Substances	GATA Transcription Factors ; GATA1 Transcription Factor ; GATA2 Transcription Factor
Language	English
Publishing date	2016-08
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	185107-x
ISSN	1873-2399 ; 0531-5573 ; 0301-472X
ISSN (online)	1873-2399
ISSN	0531-5573 ; 0301-472X
DOI	10.1016/j.exphem.2016.05.010
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Article ; Online: Heterozygous variants in GATA2 contribute to DCML deficiency in mice by disrupting tandem protein binding.

Hasegawa, Atsushi / Hayasaka, Yuki / Morita, Masanobu / Takenaka, Yuta / Hosaka, Yuna / Hirano, Ikuo / Yamamoto, Masayuki / Shimizu, Ritsuko

Communications biology

2022 Volume 5, Issue 1, Page(s) 376

Abstract: Accumulating lines of clinical evidence support the emerging hypothesis that loss-of-function mutations of GATA2 cause inherited hematopoietic diseases, including Emberger syndrome; dendritic cell, monocyte B and NK lymphoid (DCML) deficiency; and ... ...

Abstract	Accumulating lines of clinical evidence support the emerging hypothesis that loss-of-function mutations of GATA2 cause inherited hematopoietic diseases, including Emberger syndrome; dendritic cell, monocyte B and NK lymphoid (DCML) deficiency; and MonoMAC syndrome. Here, we show that mice heterozygous for an arginine-to-tryptophan substitution mutation in GATA2 (G2
MeSH term(s)	Animals ; GATA2 Transcription Factor/genetics ; Heterozygote ; Humans ; Mice ; Monocytes/metabolism ; Mutation ; Phenotype ; Protein Binding ; Receptors, Chimeric Antigen/genetics
Chemical Substances	GATA2 Transcription Factor ; GATA2 protein, human ; Gata2 protein, mouse ; Receptors, Chimeric Antigen
Language	English
Publishing date	2022-04-19
Publishing country	England
Document type	Journal Article
ISSN	2399-3642
ISSN (online)	2399-3642
DOI	10.1038/s42003-022-03316-w
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