1. Academic Validation
  2. Decreased Expression of TRPV4 Channels in HEI-OC1 Cells Induced by High Glucose Is Associated with Hearing Impairment

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

  • Yonsei Med J. 2018 Nov;59(9):1131-1137. doi: 10.3349/ymj.2018.59.9.1131.
Ying Xing  # 1 Jie Ming  # 1 Tao Liu 1 Nana Zhang 1 Dingjun Zha 2 Ying Lin 3
Affiliations

Affiliations

  • 1 Department of Endocrinology and Metabolism Disease, Xijing Hospital, Forth Military Medical University, Xi'an, China.
  • 2 Department of Otorhinolaryngology Head and Neck Surgery, Xijing Hospital, Forth Military Medical University, Xi'an, China. djzhaxian@21cn.com.
  • 3 Department of Otorhinolaryngology Head and Neck Surgery, Xijing Hospital, Forth Military Medical University, Xi'an, China. yinglinres@163.com.
  • # Contributed equally.
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

HEI-OC1 cells; TRPV4; hearing impairment; high glucose.

Figures
Products