Semaphorin 7A plays a critical role in IgE-mediated airway inflammation in mice

Mizutani, Nobuaki; Nabe, Takeshi; Yoshino, Shigefumi

doi:10.1016/j.ejphar.2015.07.004

Cited by 15 publications

(21 citation statements)

References 42 publications

(76 reference statements)

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“…Previous studies have shown that b1-integrin is associated with immunomodulatory function and plexin C1 was associated with cell adhesion, dendricity and cytoskeletal reorganization. [4][5][6][7] In our present study, we found that SEMA7A and its receptor plexin C1 were highly expressed in NSCLC A549 cells and H1299 cells. Therefore, we explored the effect of interaction between SEMA7A and plexin C1 on NSCLC A549 cell and H1299 cell migration and its related signaling pathways.…”

Section: Discussionsupporting

confidence: 56%

“…21 SEMA7A is also involved in immune responses such as modulation of T cell function, stimulation of macrophage recruitment and pro-inammatory cytokine production, regulation of chemokine expression and dendritic cell migration. [4][5][6][7][8]22,23 During the recent past years, several studies have shown that SEMA7A has effect in cancer progression. [10][11][12] SEMA7A worked through interaction with its receptor plexin C1 and b1-integrin.…”

Section: Discussionmentioning

confidence: 99%

“…As regards to the SEMA7A receptors involved in the cell migration process, several works associate b1-integrin with immunomodulatory function. [4][5][6][7] However, plexin C1 have been associated with cell adhesion, dendricity and cytoskeletal reorganization. [8][9][10] Recent studies showed that SEMA7A also has effect in cancer progression.…”

Section: Introductionmentioning

confidence: 99%

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The role of semaphorin 7A and its receptor plexin C1 in the migration of NSCLC cells

2017

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Section: Discussionsupporting

confidence: 56%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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The role of semaphorin 7A and its receptor plexin C1 in the migration of NSCLC cells

2017

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“…and online Supplement). In addition to genes cited above, SEMA7A was eosinophil-specific and may play a role in airway remodeling of asthma 28. CLC, IL5RA, SIGLEC8, SEMA7A correlated strongly to differentially methylated CpG sites in asthma 17.…”

mentioning

confidence: 87%

A novel whole blood gene expression signature for asthma, dermatitis, and rhinitis multimorbidity in children and adolescents

Lemonnier

Melén

Jiang

et al. 2020

Allergy

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Background: Allergic diseases often occur in combination (multimorbidity). Human blood transcriptome studies have not addressed multimorbidity. Large-scale gene expression data were combined to retrieve biomarkers and signaling pathways to disentangle allergic multimorbidity phenotypes. Methods: Integrated transcriptomic analysis was conducted in 1233 participants with a discovery phase using gene expression data (Human Transcriptome Array 2.0) from whole blood of 786 children from three European birth cohorts (MeDALL), and a replication phase using RNA Sequencing data from an independent cohort (EVA-PR, n = 447). Allergic diseases (asthma, atopic dermatitis, rhinitis) were considered as single disease or multimorbidity (at least two diseases), and compared with no disease. Results: Fifty genes were differentially expressed in allergic diseases. Thirty-two were not previously described in allergy. Eight genes were consistently overexpressed in all types of multimorbidity for asthma, dermatitis, and rhinitis (CLC, EMR4P, IL5RA, FRRS1, HRH4, SLC29A1, SIGLEC8, IL1RL1). All genes were replicated the in EVA-PR cohort. RT-qPCR validated the overexpression of selected genes. In MeDALL, 27 genes were differentially expressed in rhinitis alone, but none was significant for asthma or dermatitis alone. The multimorbidity signature was enriched in eosinophil-associated immune response and signal transduction. Protein-protein interaction network analysis identified IL5/JAK/STAT and IL33/ST2/IRAK/TRAF as key signaling pathways in multimorbid diseases. Synergistic effect of multimorbidity on gene expression levels was found. Conclusion: A signature of eight genes identifies multimorbidity for asthma, rhinitis, and dermatitis. Our results have clinical and mechanistic implications, and suggest that multimorbidity should be considered differently than allergic diseases occurring alone.

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“…Originally, SEMA7A was identified as neuronal guidance proteins (7). Recent studies demonstrated that SEMA7A has the effect of promoting the production of cytokines in inflammatory cells (9,10). In addition, SEMA7A also has the effect of reorganizing the cytoskeleton in several cell types and this effect is necessary for cell spreading and migration (11)(12)(13).…”

Section: Introductionmentioning

confidence: 99%

Endothelial semaphorin 7A promotes seawater aspiration-induced acute lung injury through plexin C1 and β1 integrin

Zhang

Xue²,

Liu

et al. 2017

Molecular Medicine Reports

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Inflammation and edema are two main characteristics in seawater aspiration‑induced acute lung injury (ALI). In a previous study of the authors, it was demonstrated that endothelial semaphorin 7A (SEMA7A) serves an important role in the development of seawater‑induced inflammation and edema. However, the mechanism of endothelial SEMA7A‑mediated ALI remains unclear. Therefore, the authors explored the effect of SEMA7A in rat pulmonary microvascular endothelial cells (RPMVECs) and the interaction between endothelial SEMA7A and alveolar macrophages during seawater aspiration‑induced ALI. The role of SEMA7A in endothelial permeability was detected using plexin C1 blocking antibody or SEMA7A small interfering (si)RNA. In addition, RPMVECs were co‑cultured with rat alveolar macrophage cell line‑NR8383 cells and pro‑inflammatory cytokine production was detected. Interaction between the β1 integrin and SEMA7A was detected using the β1 integrin blocking antibody or SEMA7A siRNA. Seawater stimulation induced endothelial cytoskeleton remodeling, endothelial permeability, phosphorylation of cofilin, and increased the vascular endothelial growth factor (VEGF) expression in RPMVECs. Moreover, seawater stimulation led to expression of proinflammatory cytokines and activated the nuclear factor‑κB pathway in co‑cultured cells. However, blockage with the plexin C1 antibody inhibited endothelial cytoskeleton remodeling, endothelial permeability, phosphorylation of cofilin, and treatment with SEMA7A siRNA inhibited expression of VEGF in RPMVECs. In addition, blockage with β1 integrin antibody reduced expression of proinflammatory cytokines and inhibited activation of NF‑κB in co‑culture cells. These results suggest that SEMA7A promotes seawater induced lung edema via plexin C1 and stimulates seawater induced lung inflammation via β1 integrin.

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Semaphorin 7A plays a critical role in IgE-mediated airway inflammation in mice

Cited by 15 publications

References 42 publications

The role of semaphorin 7A and its receptor plexin C1 in the migration of NSCLC cells

The role of semaphorin 7A and its receptor plexin C1 in the migration of NSCLC cells

A novel whole blood gene expression signature for asthma, dermatitis, and rhinitis multimorbidity in children and adolescents

Endothelial semaphorin 7A promotes seawater aspiration-induced acute lung injury through plexin C1 and β1 integrin

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