Hyperosmotic Stress–Induced TRPM2 Channel Activation Stimulates NLRP3 Inflammasome Activity in Primary Human Corneal Epithelial Cells | Zendy

Qinxiang Zheng | Zendy; Qiufan Tan | Zendy; Yueping Ren | Zendy; Peter S. Reinach | Zendy; Ling Li | Zendy; Chaoxiang Ge | Zendy; Jia Qu | Zendy; Wei Chen | Zendy

Open Access

Hyperosmotic Stress–Induced TRPM2 Channel Activation Stimulates NLRP3 Inflammasome Activity in Primary Human Corneal Epithelial Cells

Author(s) -

Qinxiang Zheng,

Qiufan Tan,

Yueping Ren,

Peter S. Reinach,

Ling Li,

Chaoxiang Ge,

Jia Qu,

Wei Chen

Publication year - 2018

Publication title -

investigative ophthalmology and visual science

Language(s) - Uncategorized

Resource type - Journals

SCImago Journal Rank - 1.935

H-Index - 218

eISSN - 1552-5783

pISSN - 0146-0404

DOI - 10.1167/iovs.18-23965

Subject(s) - trpm2 , inflammasome , oxidative stress , gene knockdown , chemistry , osmotic concentration , transfection , microbiology and biotechnology , apoptosis , biology , receptor , biochemistry , transient receptor potential channel , gene

The purpose of this study was to determine whether either a hyperosmotic or oxidative stress induces NLRP3 inflammasome activation and increases in bioactive IL-1β secretion through transient receptor potential melastatin 2 (TRPM2) activation in primary human corneal epithelial cells (PHCECs).

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