Role of IL-4 in bone marrow driven dysregulated angiogenesis and age-related macular degeneration

Baba, Takashi; Miyazaki, Dai; Inata, Kodai; Uotani, Ryu; Miyake, Hitomi; Sasaki, Shin‐ichi; Shimizu, Yumiko; Inoue, Yoshitsugu; Nakamura, Kazuomi

doi:10.7554/elife.54257

Cited by 24 publications

(24 citation statements)

References 39 publications

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“…These PSNs potentially release CCL2 that signals to monocytes and dendritic cells, as well as IL18 that signals back to basophils (Figure 4B, C and S6). Indeed, IL4 has been shown to induce CCL2 release from bone-marrow derived endothelial progenitor cells (Baba et al, 2020), and similar mechanism may exist in PSNs.…”

Section: Psn Sensing and Signaling Inflammationmentioning

confidence: 94%

Molecular, anatomical, and functional organization of lung interoceptors

Liu

Arce

Krasnow

2021

Preprint

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Interoceptors, sensory neurons that monitor internal organs and states, are essential for physiological homeostasis and generating internal perceptions. Here we describe a comprehensive transcriptomic atlas of interoceptors of the mouse lung, defining 10 molecular subtypes that differ in developmental origin, myelination, receptive fields, terminal morphologies, and cell contacts. Each subtype expresses a unique but overlapping combination of sensory receptors that detect diverse physiological and pathological stimuli, and each can signal to distinct sets of lung cells including immune cells, forming a local neuroimmune interaction network. Functional interrogation of two mechanosensory subtypes reveals exquisitely-specific homeostatic roles in breathing, one regulating inspiratory time and the other inspiratory flow. The results suggest that lung interoceptors encode diverse and dynamic sensory information rivaling that of canonical exteroceptors, and this information is used to drive myriad local cellular interactions and enable precision control of breathing, while providing only vague perceptions of organ states.

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Section: Psn Sensing and Signaling Inflammationmentioning

confidence: 94%

Molecular, anatomical, and functional organization of lung interoceptors

Liu

Arce

Krasnow

2021

Preprint

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“…This study concluded that, although VEGF-A was upregulated, pulmonary angiogenesis was diminished in the absence of IL-4, confounding the role of IL-4 in hypoxia-induced angiogenesis from earlier reports [32]. Later studies have also indicated that IL-4 promotes angiogenesis via direct effects on endothelial cells [33]. One such study focused on age-related macular degeneration and concluded that IL-4 promoted choroidal neovascularization both by directly stimulating tube formation in endothelial progenitor cells and by inducing vasculogenesis through bone marrow-derived endothelial progenitor cells [33].…”

Section: Anti-inflammatory Cytokinesmentioning

confidence: 85%

“…Later studies have also indicated that IL-4 promotes angiogenesis via direct effects on endothelial cells [33]. One such study focused on age-related macular degeneration and concluded that IL-4 promoted choroidal neovascularization both by directly stimulating tube formation in endothelial progenitor cells and by inducing vasculogenesis through bone marrow-derived endothelial progenitor cells [33]. Another study in an atopic dermatitis model showed that IL-4 dysregulates the expression of microRNAs involved in angiogenesis which may contribute to the excessive angiogenesis seen in disease pathogenesis [34].…”

Section: Anti-inflammatory Cytokinesmentioning

confidence: 99%

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Challenging the Paradigm: Anti-Inflammatory Interleukins and Angiogenesis

Peluzzo

Autieri

2022

Cells

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Angiogenesis is a vital biological process, and neovascularization is essential for the development, wound repair, and perfusion of ischemic tissue. Neovascularization and inflammation are independent biological processes that are linked in response to injury and ischemia. While clear that pro-inflammatory factors drive angiogenesis, the role of anti-inflammatory interleukins in angiogenesis remains less defined. An interleukin with anti-inflammatory yet pro-angiogenic effects would hold great promise as a therapeutic modality to treat many disease states where inflammation needs to be limited, but revascularization and reperfusion still need to be supported. As immune modulators, interleukins can polarize macrophages to a pro-angiogenic and reparative phenotype, which indirectly influences angiogenesis. Interleukins could also potentially directly induce angiogenesis by binding and activating its receptor on endothelial cells. Although a great deal of attention is given to the negative effects of pro-inflammatory interleukins, less is described concerning the potential protective effects of anti-inflammatory interleukins on various disease processes. To focus this review, we will consider IL-4, IL-10, IL-13, IL-19, and IL-33 to be anti-inflammatory interleukins, all of which have recognized immunomodulatory effects. This review will summarize current research concerning anti-inflammatory interleukins as potential drivers of direct and indirect angiogenesis, emphasizing their role in future therapeutics.

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“…EPCs capable of contributing to capillary formation can be derived from bone marrow cells [ 61 , [63] , [64] , [65] , [66] ]. Baba aet al reported that bone marrow-derived cells can differentiate into ECs within the CNV lesion [67] . Feng aet al recently reported [68] that there is no evidence for erythromyeloid progenitor-derived vascular endothelial cells in multiple organs during development.…”

Section: Discussionmentioning

confidence: 99%

Myeloid lineage contributes to pathological choroidal neovascularization formation via SOCS3

et al. 2021

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Background Pathological neovascularization in neovascular age-related macular degeneration (nAMD) is the leading cause of vision loss in the elderly. Increasing evidence shows that cells of myeloid lineage play important roles in controlling pathological endothelium formation. Suppressor of cytokine signaling 3 (SOCS3) pathway has been linked to neovascularization. Methods We utilised a laser-induced choroidal neovascularization (CNV) mouse model to investigate the neovascular aspect of human AMD. In several cell lineage reporter mice, bone marrow chimeric mice and Socs3 loss-of-function (knockout) and gain-of-function (overexpression) mice, immunohistochemistry, confocal, and choroidal explant co-culture with bone marrow-derived macrophage medium were used to study the mechanisms underlying pathological CNV formation via myeloid SOCS3. Findings SOCS3 was significantly induced in myeloid lineage cells, which were recruited into the CNV lesion area. Myeloid S ocs3 overexpression inhibited laser-induced CNV, reduced myeloid lineage-derived macrophage/microglia recruitment onsite, and attenuated pro-inflammatory factor expression. Moreover, SOCS3 in myeloid regulated vascular sprouting ex vivo in choroid explants and SOCS3 agonist reduced in vivo CNV. Interpretation These findings suggest that myeloid lineage cells contributed to pathological CNV formation regulated by SOCS3. Funding This project was funded by NIH/NEI (R01EY030140, R01EY029238), BrightFocus Foundation, American Health Assistance Foundation (AHAF), and Boston Children's Hospital Ophthalmology Foundation for YS and the National Institutes of Health/National Heart, Lung and Blood Institute (U01HL098166) for PZ.

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Role of IL-4 in bone marrow driven dysregulated angiogenesis and age-related macular degeneration

Cited by 24 publications

References 39 publications

Molecular, anatomical, and functional organization of lung interoceptors

Molecular, anatomical, and functional organization of lung interoceptors

Challenging the Paradigm: Anti-Inflammatory Interleukins and Angiogenesis

Myeloid lineage contributes to pathological choroidal neovascularization formation via SOCS3

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