Fig. 6

In vivo GNAZ knockdown induces retinal damages that mimic blue light exposure. To study the role of GNAZ, the retinal GNAZ was silenced by ITV injection of shRNA, subjected to ophthalmology examination (Additional file 1: Figure S2B). A Representative images and the quantified histogram authenticated the knockdown of GNAZ in the right eye (shRNA-injected), as compared to that in the left eye (sham treatment). The right eye also exhibited an increased phospho-ADAM17 and a reduced CLDN5 protein level. (*p < 0.05, **p < 0.01, ***p < 0.001, indicates statistical difference from the right eye of control mice). B Several exudates were observed in FP of GNAZ-KD group. By FFA, the leaking fluorescein were found in the fundus field, corresponding to the quantification data C. OCT-scanning proved the exudates in GNAZ-KD group. D Retinal thickness computed by the software showed an atrophy of total retina by GNAZ-KD, as compared to that in the control. The thickness of retinal sublayers was summarized in Table 3. E In GNAZ-KD, the recording ERG a- and b-wave were obviously attenuated in amplitude F and delayed in implicit time G. (*p < 0.05, **p < 0.01, ***p < 0.001, indicates statistical difference from the sham eye). These data strongly indicate that GNAZ might be the gatekeeper of retinal electrophysiology function in vivo. GNAZ-KD induced retinopathy mimic blue light exposure