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Published on: November 21, 2012
Glial-derived neurotrophic factor promotes aberrant basal cell hyperplasia in nasal polyps
Yilin Hou1, Lin Sun2, Mengqi Su3
1Otorhinolaryngology, Peking University Shenzhen Hospital, Shenzhen Peking University-The Hong Kong University of Science and Technology Medical Center, Guangdong province, China; Department of Otorhinolaryngology, First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, PR China; Department of Allergy, First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, PR China; Otorhinolaryngology Institute of Sun Yat-sen University, Guangzhou, Guangdong, PR China; Guangzhou Key Laboratory of Otorhinolaryngology, Guangzhou, Guangdong, PR China.
Background:
Neurotrophins are elevated in nasal polyps (NPs) and/or allergies, exerting neurogenic inflammatory effects. Non-classical glial-derived neurotrophic factor (GDNF) family ligands (GFLs) remain poorly understood in chronic rhinosinusitis with NP (CRSwNP).
Methods:
GDNF expression was analyzed in 67 nasal fluids (NFs) and 44 tissues via proteomic, transcriptomic, and immunohistochemical assays. Immunofluorescence co-staining identified GDNF and p63 + basal cells (BCs). Functional studies in human nasal epithelial cells (HNECs) assessed GDNF's affects on proliferation and barrier integrity. Bioinformatics identified regulatory networks and drug candidates.
Results:
GDNF existed in NFs and tissues of CRSwNP, with higher abundance in eosinophilic NPs. P63 + BCs expression positively correlates with GDNF levels. GDNF potently activated MAPK/PI3K/Akt signaling in HNECs and induced Ki-67+/p63 + cells proliferation, while reduced distribution of claudin-1 at junctions. miR-204-5p/211-5p and two FDA-approved neuroactive drugs were predicted as GDNF modulators.
Conclusions:
GDNF drives aberrant epithelial remodeling in CRSwNP via MAPK/PI3K signaling, highlighting its therapeutic potential for refractory disease.
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