Transcription factor induction of vascular blood stem cell niches in vivo

Hagedorn, Elliott J.; Perlin, Julie R.; Freeman, Rebecca J.; Wattrus, Samuel J.; Han, Tianxiao; Mao, Clara; Kim, Ji Wook; Fernández-Maestre, Inés; Daily, Madeleine L.; D'Amato, Christopher R.; Fairchild, Michael J.; Riquelme, Raquel; Li, Brian; Ragoonanan, Dana A.V.E.; Enkhbayar, Khaliun; Henault, Emily L.; Wang, Helen G.; Redfield, Shelby E.; Collins, Samantha H.; Lichtig, Asher; Yang, Song; Zhou, Yi; Kunar, Balvir; Gómez-Salinero, Jesús M.; Dinh, Thanh; Pan, Junliang; Holler, Karoline; Feldman, Henry A.; Butcher, Eugene C.; Oudenaarden, Alexander van; Rafii, Shahin; Junker, Jan Philipp; Zon, Leonard I.

doi:10.1016/j.devcel.2023.04.007

Cited by 8 publications

(2 citation statements)

References 75 publications

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“…The latest research has demonstrated that the upregulation of specific TFs alters the ECs niches. Overexpression of TFs SoxF, Ets, and NHR induces ectopic ECs that support and recruit hematopoietic stem/progenitor cells, which normally tend to be stationary under the promotion of VECs ( 32 , 33 ). These studies will better understand the effect of vascular niche on homeostasis and regeneration of blood stem cells.…”

Section: Tfs In Vascular Biologymentioning

confidence: 99%

The role of transcription factors in the pathogenesis and therapeutic targeting of vascular diseases

Hu,

Du,

et al. 2024

Front. Cardiovasc. Med.

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Transcription factors (TFs) constitute an essential component of epigenetic regulation. They contribute to the progression of vascular diseases by regulating epigenetic gene expression in several vascular diseases. Recently, numerous regulatory mechanisms related to vascular pathology, ranging from general TFs that are continuously activated to histiocyte-specific TFs that are activated under specific circumstances, have been studied. TFs participate in the progression of vascular-related diseases by epigenetically regulating vascular endothelial cells (VECs) and vascular smooth muscle cells (VSMCs). The Krüppel-like family (KLF) TF family is widely recognized as the foremost regulator of vascular diseases. KLF11 prevents aneurysm progression by inhibiting the apoptosis of VSMCs and enhancing their contractile function. The presence of KLF4, another crucial member, suppresses the progression of atherosclerosis (AS) and pulmonary hypertension by attenuating the formation of VSMCs-derived foam cells, ameliorating endothelial dysfunction, and inducing vasodilatory effects. However, the mechanism underlying the regulation of the progression of vascular-related diseases by TFs has remained elusive. The present study categorized the TFs involved in vascular diseases and their regulatory mechanisms to shed light on the potential pathogenesis of vascular diseases, and provide novel insights into their diagnosis and treatment.

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Section: Tfs In Vascular Biologymentioning

confidence: 99%

The role of transcription factors in the pathogenesis and therapeutic targeting of vascular diseases

Hu,

Du,

et al. 2024

Front. Cardiovasc. Med.

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“…101 The hematopoetic stem and progenitor cells later move from the caudal hematopoietic tissue to the kidney 102 (reviewed in detail 103,104 ). In the kidney, hematopoetic stem and progenitor cells continue to supply the organism with blood cells 105 and can respond to metabolic changes, for example, expand as a result of hypercholesteremia. 106 Several structural differences between fish and mammalian liver architecture must be considered when establishing zebrafish as a model for human disease.…”

Section: The Livermentioning

confidence: 99%

Zebrafish ApoB-Containing Lipoprotein Metabolism: A Closer Look

Moll,

Farber

2024

ATVB

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Zebrafish have become a powerful model of mammalian lipoprotein metabolism and lipid cell biology. Most key proteins involved in lipid metabolism, including cholesteryl ester transfer protein, are conserved in zebrafish. Consequently, zebrafish exhibit a human-like lipoprotein profile. Zebrafish with mutations in genes linked to human metabolic diseases often mimic the human phenotype. Zebrafish larvae develop rapidly and externally around the maternally deposited yolk. Recent work revealed that any disturbance of lipoprotein formation leads to the accumulation of cytoplasmic lipid droplets and an opaque yolk, providing a visible phenotype to investigate disturbances of the lipoprotein pathway, already leading to discoveries in microsomal triglyceride transfer protein and ApoB (apolipoprotein B). By 5 days of development, the digestive system is functional, making it possible to study fluorescently labeled lipid uptake in the transparent larvae. These and other approaches enabled the first in vivo description of the STAB (stabilin) receptors, showing lipoprotein uptake in endothelial cells. Various zebrafish models have been developed to mimic human diseases by mutating genes known to influence lipoproteins (eg, ldlra , apoC2 ). This review aims to discuss the most recent research in the zebrafish ApoB-containing lipoprotein and lipid metabolism field. We also summarize new insights into lipid processing within the yolk cell and how changes in lipid flux alter yolk opacity. This curious new finding, coupled with the development of several techniques, can be deployed to identify new players in lipoprotein research directly relevant to human disease.

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Disturbed endothelial cell signaling in tumor progression and therapy resistance

Fischer,

Alsina-Sanchis

2024

Current Opinion in Cell Biology

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Transcription factor induction of vascular blood stem cell niches in vivo

Cited by 8 publications

References 75 publications

The role of transcription factors in the pathogenesis and therapeutic targeting of vascular diseases

The role of transcription factors in the pathogenesis and therapeutic targeting of vascular diseases

Zebrafish ApoB-Containing Lipoprotein Metabolism: A Closer Look

Disturbed endothelial cell signaling in tumor progression and therapy resistance

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