Biochemical study of molecular target therapy for retinal ganglion cell death in glaucoma

2015 Fiscal Year Final Research Report

• Project/Area Number: 25861611
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Ophthalmology
• Research Institution: Hirosaki University
• Principal Investigator: Ozaki Taku 弘前大学, 医学(系)研究科(研究院), 特任助教 (70621069)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: 緑内障 / 網膜 / 網膜神経節細胞 / アポトーシス / ペプチド医薬 / ミトコンドリア / カルパイン / アポトーシス誘導因子

Outline of Final Research Achievements

Glaucoma is a disease that damages the eye's optic nerve and retinal ganglion cells (RGC), resulting in vision loss and blindness. The purpose of the present study was to determine whether the inhibition of mitochondrial μ-calpain protects the RGC in one of the animal models of glaucoma.
I used a well-established rat model of experimental acute glaucoma, ischemia/reperfusion injury. The specific peptide inhibitor of mitochondrial μ-calpain, Tat-μCL, was used for the topical eye-drop application. I applied eye-drops containing 1 mM Tat-μCL to rats three times a day for 5 days after I/R. RGC death was determined by TUNEL assay. The change of retinal function was examined by electroretinogram (ERG).
Eye-drop application of Tat-μCL significantly prevented the RGC death. The Tat-μCL significantly inhibited the decrease of RGC. In addition, both a- and b-wave in ERG were attenuated after I/R, but the eye-drop application of Tat-μCL significantly recovered the attenuation.

Free Research Field

細胞生化学