Protective Effect of Bax Ablation Against Cell Loss in the Retinal Ganglion Layer Induced by Optic Nerve Crush in Transgenic Mice

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Bax expression is a prerequisite for retinal ganglion cell (RGC) apoptosis. Experimental studies have reported Bax protein upregulation following optic nerve transection. The stimuli that trigger apoptosis share a common executioner proteolysis cascade, including caspase-3 and poly-(adenosine diphosphate ribose) polymerase cleavage. This study sought to elucidate the role of the mitochondrial apoptotic pathway in RGCs using a Bax transgenic knockout mouse model.


The right optic nerves of 26 C57BL mice, 7 Bax−/−, 7 Bax+/−, and 12 Bax+/+, were subjected to crush injury and analyzed for apoptosis and neuronal cell loss on days 1, 3, and 21. Levels of Bax, Bcl-2, and caspase-3 messenger RNA expression were determined with real-time polymerase chain reaction.


Multiple apoptotic cells were detected in the retinas of the Bax +/+ and Bax +/− mice at days 1 and 3, but not in the Bax−/− mice. The Bax/Bcl-2 ratio was higher in the Bax+/+ than in the Bax+/− mice on day 1 (1.33 and 0.83, respectively), with a trend toward an increase on day 3 (1.47 and 1.66, respectively); Bax/Bcl-X showed the same elevation on day 1 in the wild-type mice (1.34) but decreased on day 3 (0.8). Bax gene expression was undetectable in the Bax−/− mice. Caspase-3 gene expression was higher in the Bax+/+ than in the Bax+/− mice on day 1 and dropped toward baseline on day 3. The opposite trend was noted in the Bax−/− mice.


The lack of apoptosis combined with the reduction in proapoptotic genes in the Bax−/− mice after injury compared to the Bax+/+ and Bax+/− mice suggests that Bax plays a crucial role in the induction of apoptosis. Suppression of Bax expression may reduce retinal cell loss.

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