Regulatory mechanisms of Robo4 and their effects on angiogenesis

Dai, Chang; Gong, Qiang; Cheng, Yan; Su, Guanfang

doi:10.1042/bsr20190513

Cited by 39 publications

(40 citation statements)

References 140 publications

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“…2 A , Left ). It has been demonstrated that the soluble ligand Slit2, by interacting with Robo4, can modulate endothelial permeability and integrity in the lungs ( 25 ). Therefore, we administered Slit2 daily intravenously (i.v.)…”

Section: Resultsmentioning

confidence: 99%

Capillary leakage provides nutrients and antioxidants for rapid pneumococcal proliferation in influenza-infected lower airways

Sender

Hentrich

Pathak

et al. 2020

Proc. Natl. Acad. Sci. U.S.A.

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Influenza A virus (IAV)-related mortality is often due to secondary bacterial infections, primarily by pneumococci. Here, we study how IAV-modulated changes in the lungs affect bacterial replication in the lower respiratory tract (LRT). Bronchoalveolar lavages (BALs) from coinfected mice showed rapid bacterial proliferation 4 to 6 h after pneumococcal challenge. Metabolomic and quantitative proteomic analyses demonstrated capillary leakage with efflux of nutrients and antioxidants into the alveolar space. Pneumococcal adaptation to IAV-induced inflammation and redox imbalance increased the expression of the pneumococcal chaperone/protease HtrA. Presence of HtrA resulted in bacterial growth advantage in the IAV-infected LRT and protection from complement-mediated opsonophagocytosis due to capsular production. Absence of HtrA led to growth arrest in vitro that was partially restored by antioxidants. Pneumococcal ability to grow in the IAV-infected LRT depends on the nutrient-rich milieu with increased levels of antioxidants such as ascorbic acid and its ability to adapt to and cope with oxidative damage and immune clearance.

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Section: Resultsmentioning

confidence: 99%

Capillary leakage provides nutrients and antioxidants for rapid pneumococcal proliferation in influenza-infected lower airways

Sender

Hentrich

Pathak

et al. 2020

Proc. Natl. Acad. Sci. U.S.A.

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“…To date, several downstream signals of the Robo receptor have been identified ( Ypsilanti et al, 2010 ; Blockus and Chédotal, 2016 ; Dai et al, 2019 ; Jiang et al, 2019 ; Tong et al, 2019 ). Here, we focus on two Slit-Robo-mediated signal transduction systems that are involved in cerebral cortex formation.…”

Section: Molecular Pathway Of Slit-robo Signalingmentioning

confidence: 99%

Beyond Axon Guidance: Roles of Slit-Robo Signaling in Neocortical Formation

Gonda

Namba

Hanashima

2020

Front. Cell Dev. Biol.

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The formation of the neocortex relies on intracellular and extracellular signaling molecules that are involved in the sequential steps of corticogenesis, ranging from the proliferation and differentiation of neural progenitor cells to the migration and dendrite formation of neocortical neurons. Abnormalities in these steps lead to disruption of the cortical structure and circuit, and underly various neurodevelopmental diseases, including dyslexia and autism spectrum disorder (ASD). In this review, we focus on the axon guidance signaling Slit-Robo, and address the multifaceted roles of Slit-Robo signaling in neocortical development. Recent studies have clarified the roles of Slit-Robo signaling not only in axon guidance but also in progenitor cell proliferation and migration, and the maturation of neocortical neurons. We further discuss the etiology of neurodevelopmental diseases, which are caused by defects in Slit-Robo signaling during neocortical formation.

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“…Other pathways regulating microvascular function, such as Slit-2/Roundabout (Robo4), may also be involved in the pathobiology of SM. Robo4 is expressed by endothelial cells, and when activated via Slit-2, it promotes endothelial quiescence by blocking Srcmediated VE-cadherin internalization, a key component of adherens junctions [81][82][83]. Consistent with this role, lower Slit-2 expression is associated with microvascular dysfunction and severe infections [83,84].…”

Section: Endothelial Activationmentioning

confidence: 89%

New insights into microvascular injury to inform enhanced diagnostics and therapeutics for severe malaria

Erice

Kain

2019

Virulence

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Severe malaria (SM) has high mortality and morbidity rates despite treatment with potent antimalarials. Disease onset and outcome is dependent upon both parasite and host factors. Infected erythrocytes bind to host endothelium contributing to microvascular occlusion and dysregulated inflammatory and immune host responses, resulting in endothelial activation and microvascular damage. This review focuses on the mechanisms of host endothelial and microvascular injury. Only a small percentage of malaria infections (≤1%) progress to SM. Early recognition and treatment of SM can improve outcome, but we lack triage tools to identify SM early in the course of infection. Current point-of-care pathogen-based rapid diagnostic tests do not address this critical barrier. Immune and endothelial activation have been implicated in the pathobiology of SM. We hypothesize that measuring circulating mediators of these pathways at first clinical presentation will enable early triage and treatment of SM. Moreover, that host-based interventions that modulate these pathways will stabilize the microvasculature and improve clinical outcome over that of antimalarial therapy alone. ARTICLE HISTORY

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Regulatory mechanisms of Robo4 and their effects on angiogenesis

Cited by 39 publications

References 140 publications

Capillary leakage provides nutrients and antioxidants for rapid pneumococcal proliferation in influenza-infected lower airways

Capillary leakage provides nutrients and antioxidants for rapid pneumococcal proliferation in influenza-infected lower airways

Beyond Axon Guidance: Roles of Slit-Robo Signaling in Neocortical Formation

New insights into microvascular injury to inform enhanced diagnostics and therapeutics for severe malaria

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