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http://dx.doi.org/10.3349/ymj.2018.59.9.1131

Decreased Expression of TRPV4 Channels in HEI-OC1 Cells Induced by High Glucose Is Associated with Hearing Impairment  

Xing, Ying (Department of Endocrinology and Metabolism Disease, Xijing Hospital, Forth Military Medical University)
Ming, Jie (Department of Endocrinology and Metabolism Disease, Xijing Hospital, Forth Military Medical University)
Liu, Tao (Department of Endocrinology and Metabolism Disease, Xijing Hospital, Forth Military Medical University)
Zhang, Nana (Department of Endocrinology and Metabolism Disease, Xijing Hospital, Forth Military Medical University)
Zha, Dingjun (Department of Otorhinolaryngology Head and Neck Surgery, Xijing Hospital, Forth Military Medical University)
Lin, Ying (Department of Otorhinolaryngology Head and Neck Surgery, Xijing Hospital, Forth Military Medical University)
Publication Information
Yonsei Medical Journal / v.59, no.9, 2018 , pp. 1131-1137 More about this Journal
Abstract
Purpose: Previous reports have shown that hyperglycemia-induced inhibition of transient receptor potential vanilloid sub type 4 (TRPV4), a transient receptor potential ion channel, affects the severity of hearing impairment (HI). In this study, we explored the role of TRPV4 in HI using HEI-OC1 cells exposed to high glucose (HG). Materials and Methods: HEI-OC1 cells were cultured in a HG environment (25 mM D-glucose) for 48 hours, and qRT-PCR and Western blotting were used to analyze the expression of TRPV4 at the mRNA and protein level. TRPV4 agonist (GSK1016790A) or antagonist (HC-067047) in cultured HEI-OC1 cells was used to obtain abnormal TRPV4 expression. Functional TRPV4 activity was assessed in cultured HEI-OC1 cells using the MTT assay and a cell death detection ELISA. Results: TRPV4 agonists exerted protective effects against HG-induced HI, as evidenced by increased MTT levels and inhibition of apoptosis in HEI-OC1 cells. TRPV4 overexpression significantly increased protein levels of phosphorylated p38 mitogen-activated protein kinase (p-p38 MAPK), while TRPV4 antagonists had the opposite effect. Our results indicated that TRPV4 is a hyperglycemia-related factor that can inhibit cell proliferation and promote cell apoptosis by activating the MAPK signaling pathway in HEI-OC1 cells. Conclusion: Our results show that the overexpression of TRPV4 can attenuate cell death in HEI-OC1 cells exposed to HG.
Keywords
TRPV4; high glucose; hearing impairment; HEI-OC1 cells;
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