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Constitutive expression of vascular endothelial cell growth factor (VEGF) gene family ligand and receptors on human upper and lower airway epithelial cells
Author(s) -
Lee Hyun Sil,
Kim Jean
Publication year - 2014
Publication title -
international forum of allergy and rhinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.503
H-Index - 46
eISSN - 2042-6984
pISSN - 2042-6976
DOI - 10.1002/alr.21244
Subject(s) - receptor , vascular endothelial growth factor , neuropilin 1 , biology , angiogenesis , vascular endothelial growth factor a , flow cytometry , immunology , gene expression , microbiology and biotechnology , cancer research , medicine , gene , vegf receptors , genetics
Background We previously reported that vascular endothelial cell growth factor (VEGF) is abundantly expressed by primary human nasal epithelial cells (PNECs) and functions to promote cell hyperplasia in polyposis. Therefore, we aimed to examine the full expression profile of other members of the VEGF gene family of ligands and receptors, which may play a role in cell growth and the development of chronic rhinosinusitis with nasal polyposis (CRSwNP). Methods Messenger RNA (mRNA) and protein expression of VEGF genes, receptors, and co‐receptors was examined from cultured PNECs (n = 4) and compared to that from primary human bronchial epithelial cells (PBECs; n = 4) and the BEAS2B cell line (n = 4) by real‐time polymerase chain reaction (PCR) and flow cytometry. Results We report abundant expression of VEGFA, VEGFB, and VEGFC, detected by mRNA and flow cytometric analysis on PNECs. We herein report the novel finding that there is significant expression of VEGFR1, VEGFR2, VEGFR3, and both neuropilin co‐receptors, NP1 and NP2, at baseline conditions on PNECs. Lower airway PBECs and BEAS2B cells displayed similar patterns of expression. Conclusion PNECs express high constitutive levels of the VEGF gene family homolog of ligands and receptors. Expression of multiple VEGF ligand‐receptor combinations may function as redundant pathways to promote upper and lower airway epithelial cell growth during inflammation.