Semaphorin 3E Inhibits House Dust Mite–Induced Angiogenesis in a Mouse Model of Allergic Asthma

Tatari, Nazanin; Movassagh, Hesam; Shan, Lianyu; Koussih, Latifa; Gounni, Abdelilah S.

doi:10.1016/j.ajpath.2019.01.008

Cited by 17 publications

(10 citation statements)

References 58 publications

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“…Angiogenesis [ 129 ] plays a role in pulmonary pathophysiology [ 38 , 130 , 131 ]. VEGF-A is a major mediator of angiogenesis and can be produced by several immune cells [ 33 , 55 , 56 , 104 , 132 , 133 , 134 ].…”

Section: Discussionmentioning

confidence: 99%

“…VEGF-A is a major mediator of angiogenesis and can be produced by several immune cells [ 33 , 55 , 56 , 104 , 132 , 133 , 134 ]. To our knowledge, this is the first evidence that gp120 can induce the release of angiogenic factors from HLMCs raising the possibility that these cells can contribute to angiogenesis, a process of pivotal relevance in lung pathophysiology [ 38 , 130 , 131 ]. Further studies are needed to comprehensively define the contributive role of lung mast cells to angiogenesis in pulmonary diseases (e.g., COPD, asthma, etc.)…”

Section: Discussionmentioning

confidence: 99%

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HIV gp120 Induces the Release of Proinflammatory, Angiogenic, and Lymphangiogenic Factors from Human Lung Mast Cells

et al. 2020

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Human lung mast cells (HLMCs) express the high-affinity receptor FcεRI for IgE and are involved in chronic pulmonary diseases occurring at high frequency among HIV-infected individuals. Immunoglobulin superantigens bind to the variable regions of either the heavy or light chain of immunoglobulins (Igs). Glycoprotein 120 (gp120) of HIV-1 is a typical immunoglobulin superantigen interacting with the heavy chain, variable 3 (VH3) region of human Igs. The present study investigated whether immunoglobulin superantigen gp120 caused the release of different classes of proinflammatory and immunoregulatory mediators from HLMCs. The results show that gp120 from different clades induced the rapid (30 min) release of preformed mediators (histamine and tryptase) from HLMCs. gp120 also caused the de novo synthesis of cysteinyl leukotriene C4 (LTC4) and prostaglandin D2 (PGD2) from HLMCs. Incubation (6 h) of HLMC with gp120 induced the release of angiogenic (VEGF-A) and lymphangiogenic (VEGF-C) factors from HLMCs. The activating property of gp120 was mediated through the interaction with IgE VH3+ bound to FcεRI. Our data indicate that HIV gp120 is a viral superantigen, which induces the release of different proinflammatory, angiogenic, and lymphangiogenic factors from HLMCs. These observations could contribute to understanding, at least in part, the pathophysiology of chronic pulmonary diseases in HIV-infected individuals.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

HIV gp120 Induces the Release of Proinflammatory, Angiogenic, and Lymphangiogenic Factors from Human Lung Mast Cells

et al. 2020

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“…These previous observations are in agreement with our study, in which topical application of Ac-RLYE, a VEGFR-2 antagonist, alleviated inflammatory phenotypes and AD-like symptoms in HDM-challenged mice. As it has been reported that intranasal, but not dermal, administration of HDM in mice [ 31 ] increases VEGF and VEGFR-2 expression, resulting in angiogenesis, it is reasonable to suggest that the anti-atopic effect of Ac-RLYE in the current study is probably due to the inhibition of the VEGF/VEGFR-2 system.…”

Section: Discussionmentioning

confidence: 51%

Topical Administration of a Novel Acetylated Tetrapeptide Suppresses Vascular Permeability and Immune Responses and Alleviates Atopic Dermatitis in a Murine Model

Sung

Baek

Kim

et al. 2022

IJMS

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Although the pathogenesis of atopic dermatitis (AD) remains to be fully deciphered, skin barrier abnormality and immune dysregulation are known to be involved. Recently, the vascular endothelial growth factor (VEGF)/VEGF receptor (VEGFR) system has also been implicated in the pathogenesis of this multifactorial chronic inflammatory skin disorder. Previously, we showed that a novel tetrapeptide, N-acetyl-Arg-Leu-Tyr-Glu (Ac-RLYE), inhibits angiogenesis and vascular permeability effectively by selectively antagonizing VEGFR-2. The current study aimed to investigate the pharmacological effect of Ac-RLYE on AD in vitro and in vivo. The in vitro experiments demonstrated that Ac-RLYE inhibited VEGF-induced vascular permeability in endothelial cells. Moreover, in an in vivo animal model of AD, Ac-RLYE relieved AD-like symptoms such as ear thickness and dermatitis severity scores and infiltration of immune cells, including mast cells and eosinophils. Ac-RLYE inhibited IgE secretion, restored the skin barrier protein filaggrin level, and markedly downregulated gene expression of AD-related Th1, Th2, and Th17 cytokines. Collectively, these findings suggest that Ac-RLYE would be useful for the treatment of AD and associated inflammatory skin disorders.

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“…However, clinical proof for the reducing action of anti-IgE antibodies on airway wall remodeling is missing. Semaphorin 3E was implied to reduce remodeling of airway smooth muscle cells and angiogenesis induced by house dust mite exposure in an animal model [53,54]. Overexpression of semaphorin 3E, or intranasal administration in mice, significantly reduced eosinophilic inflammation, serum IgE, and type-2-cytokine expression [55].…”

Section: Immunologic and Non-immunologic Stimulation Of Airway Wall Rmentioning

confidence: 99%

Immunologic and Non-Immunologic Mechanisms Leading to Airway Remodeling in Asthma

Fang

Sun

Roth

2020

IJMS

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Asthma increases worldwide without any definite reason and patient numbers double every 10 years. Drugs used for asthma therapy relax the muscles and reduce inflammation, but none of them inhibited airway wall remodeling in clinical studies. Airway wall remodeling can either be induced through pro-inflammatory cytokines released by immune cells, or direct binding of IgE to smooth muscle cells, or non-immunological stimuli. Increasing evidence suggests that airway wall remodeling is initiated early in life by epigenetic events that lead to cell type specific pathologies, and modulate the interaction between epithelial and sub-epithelial cells. Animal models are only available for remodeling in allergic asthma, but none for non-allergic asthma. In human asthma, the mechanisms leading to airway wall remodeling are not well understood. In order to improve the understanding of this asthma pathology, the definition of “remodeling” needs to be better specified as it summarizes a wide range of tissue structural changes. Second, it needs to be assessed if specific remodeling patterns occur in specific asthma pheno- or endo-types. Third, the interaction of the immune cells with tissue forming cells needs to be assessed in both directions; e.g., do immune cells always stimulate tissue cells or are inflamed tissue cells calling immune cells to the rescue? This review aims to provide an overview on immunologic and non-immunologic mechanisms controlling airway wall remodeling in asthma.

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Semaphorin 3E Inhibits House Dust Mite–Induced Angiogenesis in a Mouse Model of Allergic Asthma

Cited by 17 publications

References 58 publications

HIV gp120 Induces the Release of Proinflammatory, Angiogenic, and Lymphangiogenic Factors from Human Lung Mast Cells

HIV gp120 Induces the Release of Proinflammatory, Angiogenic, and Lymphangiogenic Factors from Human Lung Mast Cells

Topical Administration of a Novel Acetylated Tetrapeptide Suppresses Vascular Permeability and Immune Responses and Alleviates Atopic Dermatitis in a Murine Model

Immunologic and Non-Immunologic Mechanisms Leading to Airway Remodeling in Asthma

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