Vascular Endothelial Growth Factor Expression in Nasal Polyps of Aspirin-Intolerant Patients

Fruth, Kai; Zhu, Chengjing; Schramek, Eduard; Angermair, Johannes; Kassem, Wassim; Haxel, Boris; Schneider, Astrid; Mann, Wolf J.; Brieger, Juergen

doi:10.1001/archoto.2011.1474

Cited by 6 publications

(5 citation statements)

References 16 publications

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“…For example, we detected a possible interaction of basal EpC VEGF with receptors on endothelial cells ( Figure 4B ). This is consistent with several reports identifying increased VEGF in nasal polyp tissue ( 48 , 49 ), and in the lower airway VEGFA from EpCs has been implicated in signaling to endothelial cells to promote angiogenesis in obstructive lung disease ( 50 , 51 ). We also detected a possible interaction of endothelial cell HB-EGF (heparin-binding EGF-like growth factor) with basal EpC receptors ( Figure 4B ), which may be involved in regulating EpC tissue remodeling in CRSwNP.…”

Section: Discussionsupporting

confidence: 93%

Increased glycolysis and cellular crosstalk in eosinophilic chronic rhinosinusitis with nasal polyps

Huang,

Mandanas,

Djeddi

et al. 2024

Front. Immunol.

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IntroductionChronic rhinosinusitis (CRS) is a chronic inflammatory disease of the sinonasal mucosa with distinct endotypes including type 2 (T2) high eosinophilic CRS with nasal polyps (eCRSwNP), T2 low non-eosinophilic CRS with nasal polyps (neCRSwNP), and CRS without nasal polyps (CRSsNP).MethodsGiven the heterogeneity of disease, we hypothesized that assessment of single cell RNA sequencing (scRNA-seq) across this spectrum of disease would reveal connections between infiltrating and activated immune cells and the epithelial and stromal populations that reside in sinonasal tissue.ResultsHere we find increased expression of genes encoding glycolytic enzymes in epithelial cells (EpCs), stromal cells, and memory T-cell subsets from patients with eCRSwNP, as compared to healthy controls. In basal EpCs, this is associated with a program of cell motility and Rho GTPase effector expression. Across both stromal and immune subsets, glycolytic programming was associated with extracellular matrix interactions, proteoglycan generation, and collagen formation. Furthermore, we report increased cell-cell interactions between EpCs and stromal/immune cells in eCRSwNP compared to healthy control tissue, and we nominate candidate receptor-ligand pairs that may drive tissue remodeling.DiscussionThese findings support a role for glycolytic reprograming in T2-elicited tissue remodeling and implicate increased cellular crosstalk in eCRSwNP.

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Section: Discussionsupporting

confidence: 93%

Increased glycolysis and cellular crosstalk in eosinophilic chronic rhinosinusitis with nasal polyps

Huang,

Mandanas,

Djeddi

et al. 2024

Front. Immunol.

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“…Previous study [29] demonstrated high levels of VEGF in nasal polyps enhanced proliferation by activating VEGF receptors and downstream pathways, subsequently promoting polyps formation. VEGF is a family of homodimeric proteins that consisted by six members, including VEGF-A, VEGF-B, VEGF-C, VEGF-D, VEGF-E and placenta growth factor [30].…”

Section: Discussionmentioning

confidence: 99%

“…VEGF is widely recognized as a major proangiogenic factor involved in the process of neovascularization and vascular leakage through VEGF receptor-mediated pathways in tissue remodeling [ 28 ]. Previous study [ 29 ] demonstrated high levels of VEGF in nasal polyps enhanced proliferation by activating VEGF receptors and downstream pathways, subsequently promoting polyps formation. VEGF is a family of homodimeric proteins that consisted by six members, including VEGF-A, VEGF-B, VEGF-C, VEGF-D, VEGF-E and placenta growth factor [ 30 ].…”

Section: Discussionmentioning

confidence: 99%

Different effects of allergic rhinitis on nasal mucosa remodeling in chronic rhinosinusitis with and without nasal polyps

Xiang

Zhang

et al. 2018

Eur Arch Otorhinolaryngol

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BackgroundAllergic rhinitis (AR) has been reported to be associated with chronic rhinosinusitis (CRS). The objective of this study was to investigate the effect of AR on nasal mucosa remodeling in CRS.MethodsPatients were enrolled and divided into the following groups: CRS with nasal polyps (NP) with allergic rhinitis (AR)(CRSwNPwAR; n = 20), CRS with NP without AR (CRSwNPsAR; n = 20), CRS without NP with AR (CRSsNPwAR; n = 20), CRS without NP without AR (CRSsNPsAR; n = 20), AR without CRS (AR; n = 20) and controls (n = 14). Eosinophil infiltration, mucus production, and collagen deposition were examined by hematoxylin and eosin, periodic acid schiff and masson’s trichrome staining, respectively. VEGF-A and microvessel density were detected by immunohistochemistry. The expression of remodeling markers, including TGF-β1, MMP-7, MMP-9 and TIMP-1 were measured by Western blot.ResultsThe expression of remodeling factors, including VEGF-A, CD31, CD34 and TIMP-1 were significantly increased in CRSwAR compared to CRSsAR. Goblet cell hyperplasia, as well as VEGF-A, CD31, CD34, and MMP-9 expression were significantly higher in CRSwNPwAR compared to CRSwNPsAR. However, the expression of collagen fibers, MMP-7 and TGF-β1 were significantly higher in CRSsNPwAR compared to CRSsNPsAR.ConclusionsAR could enhance the remodeling process in CRS. Moreover, AR had different effects on CRSwNP and CRSsNP.

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“…An increased level of VEGF is also found in the nasal lavage of chronic rhinosinusitis patients with nasal polyposis ( 181 ). The increased PGD 2 levels in nasal polyps of patients with chronic rhinosinusitis has been identified as a dominant factor in inducing the production of VEGF via the DP receptors, and an increased level of VEGF has been documented in nasal polyps of N-ERD patients ( 24 , 182 , 183 ). In N-ERD, overexpression of PGD 2 may explain the increase in VEGF, and suppression of VEGF production could be a potential mechanism, by which nasal polyp recurrence is reduced in N-ERD.…”

Section: Potential Mechanism Of Aspirin Actionmentioning

confidence: 99%

Aspirin Actions in Treatment of NSAID-Exacerbated Respiratory Disease

et al. 2021

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Non-steroidal Anti-inflammatory drugs (NSAID)-exacerbated respiratory disease (N-ERD) is characterized by nasal polyposis, chronic rhinosinusitis, adult-onset asthma and hypersensitive reactions to cyclooxygenase-1 (COX-1) inhibitors. Among the available treatments for this disease, a combination of endoscopic sinus surgery followed by aspirin desensitization and aspirin maintenance therapy has been an effective approach. Studies have shown that long-term aspirin maintenance therapy can reduce the rate of nasal polyp recurrence in patients with N-ERD. However, the exact mechanism by which aspirin can both trigger and suppress airway disease in N-ERD remains poorly understood. In this review, we summarize current knowledge of aspirin effects in N-ERD, cardiovascular disease, and cancer, and consider potential mechanistic pathways accounting for the effects of aspirin in N-ERD.

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Vascular Endothelial Growth Factor Expression in Nasal Polyps of Aspirin-Intolerant Patients

Cited by 6 publications

References 16 publications

Increased glycolysis and cellular crosstalk in eosinophilic chronic rhinosinusitis with nasal polyps

Increased glycolysis and cellular crosstalk in eosinophilic chronic rhinosinusitis with nasal polyps

Different effects of allergic rhinitis on nasal mucosa remodeling in chronic rhinosinusitis with and without nasal polyps

Aspirin Actions in Treatment of NSAID-Exacerbated Respiratory Disease

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