Sphingosine 1-Phosphate Receptor Signaling Establishes AP-1 Gradients to Allow for Retinal Endothelial Cell Specialization

Yanagida, K.; Engelbrecht, Eric; Niaudet, Colin; Jung, Bongnam; Gaengel, Konstantin; Holton, Kristina M.; Swendeman, Steven; Liu, Catherine H.; Levesque, Michel V.; Kuo, Andrew; Fu, Zhongjie; Smith, Lois E H; Betsholtz, Christer; Hla, Timothy

doi:10.1016/j.devcel.2020.01.016

Cited by 43 publications

(57 citation statements)

References 77 publications

(90 reference statements)

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“…These reports imply an important role for S1P1 in stabilizing sprouting angiogenesis in the retina. Consistently, S1pr1-3 triple knockout mice exhibited a disorganized retinal vascular endothelium with hyper-sprouting and a lack of vascular endothelial barrier and capillary lumens [125]. Moreover, S1pr1-3 deficient mice had insufficient blood perfusion in the retina and severe vascular structure defects due to impaired endothelial cell specialization.…”

Section: Sphingosine 1-phosphate and Ocular Neovascularizationmentioning

confidence: 78%

Lipid Signaling in Ocular Neovascularization

Terao

Kaneko

2020

IJMS

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Vasculogenesis and angiogenesis play a crucial role in embryonic development. Pathological neovascularization in ocular tissues can lead to vision-threatening vascular diseases, including proliferative diabetic retinopathy, retinal vein occlusion, retinopathy of prematurity, choroidal neovascularization, and corneal neovascularization. Neovascularization involves various cellular processes and signaling pathways and is regulated by angiogenic factors such as vascular endothelial growth factor (VEGF) and hypoxia-inducible factor (HIF). Modulating these circuits may represent a promising strategy to treat ocular neovascular diseases. Lipid mediators derived from membrane lipids are abundantly present in most tissues and exert a wide range of biological functions by regulating various signaling pathways. In particular, glycerophospholipids, sphingolipids, and polyunsaturated fatty acids exert potent pro-angiogenic or anti-angiogenic effects, according to the findings of numerous preclinical and clinical studies. In this review, we summarize the current knowledge regarding the regulation of ocular neovascularization by lipid mediators and their metabolites. A better understanding of the effects of lipid signaling in neovascularization may provide novel therapeutic strategies to treat ocular neovascular diseases and other human disorders.

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Section: Sphingosine 1-phosphate and Ocular Neovascularizationmentioning

confidence: 78%

Lipid Signaling in Ocular Neovascularization

Terao

Kaneko

2020

IJMS

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“…In retinal vascular development, the genome-wide accessibility of AP-1-binding sites is epigenetically controlled by sphingosine-1-phosphate (S1P) signaling. This process alters the chromatin composition of the AP-1-binding site to become closed and inaccessible, resulting in the inhibition of JunB-related gene expression during vascular maturation in the mouse retina [ 68 ].…”

Section: Ap-1 Transcription Factor Junb In Angiogenesismentioning

confidence: 99%

“…JunB is reportedly upregulated in tip cells at the angiogenic frontier and contributes to vascular development in mouse embryonic skin [ 26 ] and retinal vasculatures [ 68 ] ( Figure 1 ). The induction of JunB expression is temporal and spatial in tip cells at the angiogenic frontier or at the branching points during vascular development.…”

Section: Ap-1 Transcription Factor Junb In Angiogenesismentioning

confidence: 99%

Emerging Role of AP-1 Transcription Factor JunB in Angiogenesis and Vascular Development

Yoshitomi

Ikeda

Saito-Takatsuji

et al. 2021

IJMS

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Blood vessels are essential for the formation and maintenance of almost all functional tissues. They play fundamental roles in the supply of oxygen and nutrition, as well as development and morphogenesis. Vascular endothelial cells are the main factor in blood vessel formation. Recently, research findings showed heterogeneity in vascular endothelial cells in different tissue/organs. Endothelial cells alter their gene expressions depending on their cell fate or angiogenic states of vascular development in normal and pathological processes. Studies on gene regulation in endothelial cells demonstrated that the activator protein 1 (AP-1) transcription factors are implicated in angiogenesis and vascular development. In particular, it has been revealed that JunB (a member of the AP-1 transcription factor family) is transiently induced in endothelial cells at the angiogenic frontier and controls them on tip cells specification during vascular development. Moreover, JunB plays a role in tissue-specific vascular maturation processes during neurovascular interaction in mouse embryonic skin and retina vasculatures. Thus, JunB appears to be a new angiogenic factor that induces endothelial cell migration and sprouting particularly in neurovascular interaction during vascular development. In this review, we discuss the recently identified role of JunB in endothelial cells and blood vessel formation.

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“…It has been demonstrated that glycolysis intermediates (eg lactate and succinate) and glycolytic enzymes (eg fructose‐6‐phosphate‐2 kinase and fructose‐2,6‐diphosphatase 3) are implicated in the regulation of angiogenesis 60 . Besides this, S1PRs have a role in the regulation of VEGF‐mediated angiogenesis (co‐ordination function) 61 . Together, S1PRs may harbour broad effects on the intestinal angiogenesis of IBD by regulating ROS, ER stress, glycolysis, VEGF signal pathway and other processes, and hence, more understanding of their specific mechanisms is of great significance to the prevention and treatment of IBD (Figure 2).…”

Section: S1prs and Intestinal Angiogenesis In Ibdmentioning

confidence: 99%

Role of sphingosine‐1‐phosphate receptors in vascular injury of inflammatory bowel disease

Wang

Chen

Xiang

et al. 2021

J Cellular Molecular Medi

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Sphingosine‐1‐phosphate receptors (S1PRs) have an impact on the intestinal inflammation of inflammatory bowel disease (IBD) by regulating lymphocyte migration and differentiation. S1PR modulators as an emerging therapeutic approach are being investigated for the treatment of IBD. However, the role of S1PRs in intestinal vessels has not drawn much attention. Intestinal vascular damage is one of the major pathophysiological features of IBD, characterized by increased vascular density and impaired barrier function. S1PRs have pleiotropic effects on vascular endothelial cells, including proliferation, migration, angiogenesis and barrier homeostasis. Mounting evidence shows that S1PRs are abnormally expressed on intestinal vascular endothelial cells in IBD. Unexpectedly, S1PR modulators may damage intestinal vasculature, for example increase intestinal bleeding; therefore, S1PRs are thought to be involved in the regulation of intestinal vascular function in IBD. However, little is understood about how S1PRs regulate intestinal vascular function and participate in the initiation and progression of IBD. In this review, we summarize the pathogenic role of S1PRs in and the underlying mechanisms behind the intestinal vascular injury in IBD in order for improving IBD practice including S1PR‐targeted therapies.

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Sphingosine 1-Phosphate Receptor Signaling Establishes AP-1 Gradients to Allow for Retinal Endothelial Cell Specialization

Cited by 43 publications

References 77 publications

Lipid Signaling in Ocular Neovascularization

Lipid Signaling in Ocular Neovascularization

Emerging Role of AP-1 Transcription Factor JunB in Angiogenesis and Vascular Development

Role of sphingosine‐1‐phosphate receptors in vascular injury of inflammatory bowel disease

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