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Yuki Iwata, Satoshi Inagaki, Wataru Morozumi, Shinsuke Nakamura, Masamitsu Shimazawa, Hideaki Hara; The effect of GDF15 on the neurite outgrowth in retinal ganglion cells.. Invest. Ophthalmol. Vis. Sci. 2019;60(9):624.
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© ARVO (1962-2015); The Authors (2016-present)
Growth differentiation factor 15 (GDF15) is reported to be increased in mouse retina after optic nerve crush and in aqueous humor of primary open angle glaucoma (POAG) patients. However, the role of GDF15 on retinal ganglion cells (RGCs) survival is not understood. The purpose of this study was to elucidate the role of GDF15 on RGCs by using mouse optic nerve crush model and primary culture of rat RGCs.
To induce RGC degeneration, optic nerve was crushed at 0.5 to1.5 mm posterior to the mouse eye under anesthesia (i.p.) with a mixture of 120 mg/kg ketamine and 6 mg/kg xylazine. The expression of GDF15 was measured by using Western blotting. Purified rat RGCs were isolated on postnatal day 7 from retinas that were dissociated with MACS dissociation kit. After incubating for 24 h, the RGCs were exposed to 0.1, 1.0 μg/ml recombinant human GDF15 for 72 h. The neurite of RGC was evaluated using anti-Tuj1 antibody.
GDF15 was expressed in especially ganglion cell layer (GCL) of the retina and optic nerve head. Although the precursor GDF15 (40kDa) was not changed, the mature GDF15 (25kDa) was upregulated in the retina and optic nerve at 1, 3 and 7 days after optic nerve crush. GDF15 promoted neurite outgrowth of primary rat RGCs in a concentration-dependent manner.
These findings indicate that mature GDF15 was upregulated after optic nerve crush and promoted neurite outgrowth of primary rat RGCs, suggesting that GDF15 has the neuroprotective effect on RGCs. Therefore, GDF15 may be one of novel therapeutic targets in RGC degenerative diseases.
This abstract was presented at the 2019 ARVO Annual Meeting, held in Vancouver, Canada, April 28 - May 2, 2019.
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