Vascular endothelial growth factor receptor 1 expression in nasal polyp tissue
Background Edema represents a key feature of nasal polyp (NP) disease. Members of the vascular endothelial growth factor (VEGF) family may be involved, but the precise role of VEGF‐A, VEGF‐B, placental growth factor (PlGF), and their receptors VEGFR1 and VEGFR2 in NP edema formation remains elusive....
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Veröffentlicht in: | Allergy (Copenhagen) 2014-02, Vol.69 (2), p.237-245 |
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Sprache: | eng |
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Zusammenfassung: | Background
Edema represents a key feature of nasal polyp (NP) disease. Members of the vascular endothelial growth factor (VEGF) family may be involved, but the precise role of VEGF‐A, VEGF‐B, placental growth factor (PlGF), and their receptors VEGFR1 and VEGFR2 in NP edema formation remains elusive.
Objective
Exploring the expression of VEGF family members and their receptors and their correlation with clinical, radiological, and edema markers in NP.
Methods
The expression of VEGF‐A, VEGF‐B, PlGF, VEGFR1, and VEGFR2 was measured in NP (n = 23) and control tissue (n = 22) at mRNA and protein level. Edema was evaluated by measuring albumin levels and wet/dry ratios. Computed tomography (CT) scans were scored using the Lund‐Mackay scoring system. IL‐5 mRNA expression was determined by real‐time RT‐PCR. Cell suspensions from NP (n = 10) and control tissue (n = 12) were stimulated in vitro with IL‐1β or TNFα.
Results
mRNA expression of VEGFR1 and VEGF‐B was significantly higher in NP compared with control tissue. Expression levels of VEGF‐B and VEGFR1 significantly correlated with NP albumin content (VEGF‐B: P = 0.0208; VEGFR1: P = 0.0293), CT scan scores (VEGF‐B: P = 0.0075; VEGFR1: P = 0.0068), and IL‐5 mRNA (VEGF‐B: P = 0.0027; VEGFR1: P = 0.0001). In vitro stimulation of control and NP tissue cell suspensions with IL‐1β or TNFα significantly reduced the expression of VEGFR2 in control tissue, without altering VEGFR1 and VEGF‐B expression. hVEGF‐B induced nitric oxide production in NP macrophages (P |
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ISSN: | 0105-4538 1398-9995 |
DOI: | 10.1111/all.12277 |