A novel role for <i>Lyl1</i> in primitive erythropoiesis

Chiu, Sung Kai; Saw, Jesslyn; Huang, Yizhou; Sonderegger, Stefan Eugen; Wong, Nicholas C.; Powell, David R.; Beck, Dominic; Pimanda, John E.; Tremblay, Cédric; Curtis, David J.

doi:10.1242/dev.162990

Cited by 15 publications

(17 citation statements)

References 38 publications

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“…Up‐regulation of platelet‐activating genes was accompanied by the enrichment of genes selective for erythropoiesis, including lymphoblastic leukemia 1 (2.6‐fold) and translocated in leukemia 1 (TAL1; 1.9‐fold) transcription factors that are coexpressed in erythroid lineage progenitors (Fig. B) . Other erythroid‐selective genes included aminolevulinate synthase 2 (ALAS2; 5.3‐fold) and erythroid Kruppel‐like factor (KLF) 1 (2.8‐fold), which mediate erythrocyte differentiation .…”

Section: Resultsmentioning

confidence: 99%

“…5B). (22,23) Other erythroid-selective genes included aminolevulinate synthase 2 (ALAS2; 5.3-fold) and erythroid Kruppellike factor (KLF) 1 (2.8-fold), which mediate erythrocyte differentiation. (23,24) Also up-regulated were dematin actin binding protein (DNMNT; 2.7-fold) and EBP42 (3.5-fold), which maintain the structural integrity and function of erythrocytes.…”

Section: Peak 2: Activation Of the Complement System And Ecm Remodelingmentioning

confidence: 99%

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Profiling Gene Programs in the Blood During Liver Regeneration in Living Liver Donors

et al. 2019

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The human liver’s capacity to rapidly regenerate to a full‐sized functional organ after resection has allowed successful outcomes for living donor liver transplantation (LDLT) procedures. However, the ability to detect and track physiological changes occurring during liver regeneration after resection and throughout the restoration process is still lacking. We performed a comprehensive whole‐transcriptome RNA sequencing analysis of liver and circulating blood tissue from 12 healthy LDLT donors to define biomarker signatures for monitoring physiological activities during liver regeneration at 14 time points for up to a 1‐year procedural follow‐up. LDLT donor liver tissue differentially expressed 1238 coding and noncoding genes after resection, and an additional 1260 genes were selectively regulated after LDLT. A total of 15,011 RNA transcript species were identified in the blood in response to liver resection. The transcripts most highly regulated were sequentially expressed within 3 distinct peaks that correlated with sets of functional genes involved in the induction of liver resection–specific innate immune response (peak 1), activation of the complement system (peak 2), and platelet activation and erythropoiesis (peak 3). Each peak corresponded with progressive phases of extracellular matrix degradation, remodeling, and organization during liver restoration. These processes could be tracked by distinct molecular signatures of up‐regulated and down‐regulated gene profiles in the blood during phases of liver repair and regeneration. In conclusion, the results establish temporal and dynamic transcriptional patterns of gene expression following surgical liver resection that can be detected in the blood and potentially used as biomarker signatures for monitoring phases of liver regeneration.

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Section: Resultsmentioning

confidence: 99%

Section: Peak 2: Activation Of the Complement System And Ecm Remodelingmentioning

confidence: 99%

Profiling Gene Programs in the Blood During Liver Regeneration in Living Liver Donors

et al. 2019

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“…Specifically, disruption of LYL1 activity in mice impairs the long‐term hematopoietic reconstitution capacity and maintenance of early T lineage progenitors, and partially blocks B lymphocyte differentiation 17,18 . More recently, Chiu et al demonstrated that Lyl1 can maintain primitive erythropoiesis and compensate for the loss of Scl (another bHLH family member) in megakaryopoiesis 19,20 . LYL1 is also required for the maturation and stabilization of endothelial adherens junctions in newly formed vessels 16,21 .…”

Section: Introductionmentioning

confidence: 99%

“…17,18 More recently, Chiu et al demonstrated that Lyl1 can maintain primitive erythropoiesis and compensate for the loss of Scl (another bHLH family member) in megakaryopoiesis. 19,20 LYL1 is also required for the maturation and stabilization of endothelial adherens junctions in newly formed vessels. 16,21 Consequently, blood vessels in the lung of young adult Lyl1 −/− mice cannot form a functional endothelial barrier, leading to vascular leakiness.…”

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In Lyl1 −/− mice, adipose stem cell vascular niche impairment leads to premature development of fat tissues

et al. 2020

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Lyl1 encodes a hematopoietic- and endothelial-specific bHLH transcription factor. Lyl1-deficient mice are viable, but they display mild hematopoietic and vascular defects. Specifically, LYL1 is required for the maturation and stabilization of blood vessel endothelial adherens junctions. Here, we report that young adult Lyl1−/− mice exhibit transient overweight associated with general expansion of adipose tissue, without signs of metabolic disorder and unrelated to food intake. The increased fat tissue development in Lyl1−/− mice resulted from earlier differentiation of adipose stem cells (ASCs) into adipocytes through noncell autonomous mechanisms. Specifically, we found that in Lyl1−/− mice, the adipose tissue vascular structures are immature, as indicated by their high permeability, reduced coverage by pericytes, lower recruitment of VE-cadherin and ZO1 at cell junctions, and more prone to angiogenesis. Together, our data show that in Lyl1−/− mice, the impaired vascular compartment of the adipose niche promotes ASC differentiation, leading to early adipocyte expansion and premature ASC depletion. Our study highlights the major structural role of the adipose tissue vascular niche in coordinating stem cell self-renewal and differentiation into adipocytes.

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“…demonstrated that Lyl1 can maintain primitive erythropoiesis and compensate for loss of Scl (a LYL1 co-member of bHLH family) in megakaryopoiesis [19,20]. LYL1 is also required for the maturation and stabilization of endothelial adherens junctions of newly formed vessels [16,21].…”

Section: Introductionmentioning

confidence: 99%

InLyl1^-/-mice, adipose stem cell vascular niche impairment leads to premature development of fat tissues

Hussain

Kebriti

Deleuze

et al. 2020

Preprint

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Lymphoblastic leukemia-derived sequence 1 (Lyl1) encodes a hematopoietic-and endothelial-specific transcriptional factor. Lyl1-deficient mice are viable, but they display mild hematopoietic and vascular defects. Here, we report that young Lyl1 -/mice exhibit transient obesity associated with general expansion of adipose tissues and unrelated to food intake.The increased fat tissue development in Lyl1 -/mice resulted from an earlier adipocyte differentiation of adipose stem cells (ASCs) through non-cell autonomous mechanisms.Specifically, we found that in Lyl1 -/mice, the vascular structures of adipose tissues are unstable, more prone to angiogenesis and, consequently, cannot maintain adipose progenitors in the niche vessel wall. Together, our data show that in Lyl1 -/mice, the impaired vascular compartment of the adipose niche promotes uncontrolled ASC activation and differentiation, leading to early adipocyte expansion and premature depletion of ASCs. Our study highlights the major structural role of the adipose tissue vascular niche in coordinating stem cell self-renewal and differentiation into adipocytes.

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A novel role for Lyl1 in primitive erythropoiesis

Cited by 15 publications

References 38 publications

Profiling Gene Programs in the Blood During Liver Regeneration in Living Liver Donors

Profiling Gene Programs in the Blood During Liver Regeneration in Living Liver Donors

In Lyl1 −/− mice, adipose stem cell vascular niche impairment leads to premature development of fat tissues

InLyl1^-/-mice, adipose stem cell vascular niche impairment leads to premature development of fat tissues

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A novel role for Lyl1 in primitive erythropoiesis

Cited by 15 publications

References 38 publications

Profiling Gene Programs in the Blood During Liver Regeneration in Living Liver Donors

Profiling Gene Programs in the Blood During Liver Regeneration in Living Liver Donors

In Lyl1 −/− mice, adipose stem cell vascular niche impairment leads to premature development of fat tissues

InLyl1-/-mice, adipose stem cell vascular niche impairment leads to premature development of fat tissues

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InLyl1^-/-mice, adipose stem cell vascular niche impairment leads to premature development of fat tissues