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Min Ji, Huaijin Guan; Increased expression of P2X7 receptor induced by DHPG in retinal ganglion cells. Invest. Ophthalmol. Vis. Sci. 2017;58(8):4608.
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© ARVO (1962-2015); The Authors (2016-present)
To determine the direct effect and the possible mechanism of DHPG, an mGluR I agonist, to retinal ganglion cells.
DHPG was intravitreal injected into the left eyes of rats. The apoptosis of RGCs was determined by Retrograde Labeling and Counting of RGCs and TUNEL stain in cultured RGCs. Expression of mGluR I (mGlu1R,mGlu5R) and P2X7R protein was determined by immunohistochemistry and Western blot analysis. Mixed culture of retinal neurons were prepared for the detection of the expression of P2X7R and the ATP current. Whole-cell patch clamp was introduced to detect the change of the ATP current of RGCs.
The number of RGCs significantly decreased in retinal of rats with DHPG intraviteal injection and partly blocked by BBG, the antagonist of P2X7 receptor. TUNEL positive cells increased in cultured RGCs with the presence of DHPG and partly blocked by BBG. Our previous study showed the activation might cause the apoptosis of RGCs. P2X7 receptor, mGluR1 and mGluR5 were all expressed in the ganglion cell layer(GCL) in normal retinal slice and in cultured RGCs. DHPG could increase the expression of P2X7R both in vivo and in vitro, and both MPMQ (the mGluR1 antagonist) and MPEP (the mGluR5 antagonist) could inhibit the effects. In cultured RGCs, the ATP current did not change with DHPG perfusion, while the ATP current increased with the presence of DHPG for 2 days in the culture solution. The increased ATP current levels can be inhibited both by MPEP and MPMQ.
These datas demonstrated that DHPG increased the expression of P2X7 receptor through both mGluR1 and mGluR5, and finaly cause the apoptosisi of RGCs.
This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.
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