Volume 119, Issue 9 pp. 1834-1838
Original Study

Rhinovirus upregulates matrix metalloproteinase-2, matrix metalloproteinase-9, and vascular endothelial growth factor expression in nasal polyp fibroblasts

Jong Hwan Wang MD

Jong Hwan Wang MD

Department of Otolaryngology, Asan Medical Center, University of Ulsan, College of Medicine, Seoul, South Korea

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Hyun Ja Kwon MSc

Hyun Ja Kwon MSc

Department of Otolaryngology, Asan Medical Center, University of Ulsan, College of Medicine, Seoul, South Korea

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Yong Ju Jang MD

Corresponding Author

Yong Ju Jang MD

Department of Otolaryngology, Asan Medical Center, University of Ulsan, College of Medicine, Seoul, South Korea

Department of Otolaryngology, Asan Medical Center, University of Ulsan, College of Medicine, Pungnap-2dong, Songpa-gu, Seoul, KoreaSearch for more papers by this author
First published: 01 July 2009
Citations: 26

Abstract

Objectives/Hypothesis:

Upregulation of matrix metalloproteinase (MMP) and vascular endothelial growth factor (VEGF) has been suggested to have an important role in the pathogenesis of nasal polyps (NPs). The aim of this study was to investigate the effect of rhinovirus (RV) infection on the expression of MMPs, tissue inhibitor of metalloproteinase (TIMP)-1, and VEGF in NP fibroblasts.

Methods:

NP fibroblasts (5 × 105 cells/mL) obtained from patients with chronic rhinosinusitis with nasal polyps (CRSwNP) were infected with RV serotype 16 (RV-16) for 4 hours. The RV-16 infection was confirmed by seminested reverse transcriptase-polymerase chain reaction (RT-PCR) and in situ hybridization. After 48 hours, MMP-2, MMP-9, TIMP-1, and VEGF protein levels were measured from culture supernatants by enzyme-linked immunosorbent assay. The changes in the expression of MMP-2, MMP-9, TIMP-1, and VEGF mRNA were assayed by RT-PCR.

Results:

RV-16 infection significantly enhanced the gene and protein expressions of MMP-2, MMP-9, and VEGF in NP fibroblasts, whereas TIMP-1 expression was not significantly affected by RV-16. MMP-2, MMP-9, and VEGF protein expression increased by 2.39-, 2.99-, and 3.02-fold, respectively, in RV-infected NP fibroblasts compared to noninfected controls. RV-16 infection also significantly upregulated the expression of MMP-2, MMP-9, and VEGF mRNA by 1.27-, 1.70-, and 1.53-fold, respectively, compared to control levels.

Conclusions:

These in vitro findings suggest that RV infection may contribute to the pathogenesis of NP formation in patients with CRSwNP. Laryngoscope, 2009

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