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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)
  • Received : 2018.04.13
  • Accepted : 2018.08.10
  • Published : 2018.11.01

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

Acknowledgement

Supported by : National Natural Science Foundation of China (NSFC), Forth Military Medical University

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