AI Article Synopsis
- The combined knockout of miR-183 and miR-96 in mice leads to severe retinal degeneration, while a single knockout of miR-96 only causes developmental delays.
- Overexpressing miR-96 in the retina, even at safe levels, induces significant degeneration of photoreceptors, evidenced by various analysis techniques.
- The research indicates that proper levels of miR-96 are crucial for maintaining retinal health and suggests that overexpression triggers immune responses and microglial activation associated with degeneration.
Article Abstract
Double knockout of miR-183 and miR-96 results in retinal degeneration in mice; however, single knockout of miR-96 leads to developmental delay but not substantial retinal degeneration. To further explore the role of miR-96, we overexpressed this miRNA in mouse retinas. Interestingly, we found that overexpression of miR-96 at a safe dose results in retinal degeneration in the mouse retina. The retinal photoreceptors dramatically degenerated in the miR-96-overexpressing group, as shown by OCT, ERG and cryosectioning at one month after subretinal injection. Degenerative features such as TUNEL signals and reactive gliosis were observed in the miR-96-overexpressing retina. RNA-seq data revealed that immune responses and microglial activation occurred in the degenerating retina. Further qRT‒PCR and immunostaining experiments verified the microglial activation. Moreover, the number of microglia in the miR-96-overexpressing retinas was significantly increased. Our findings demonstrate that appropriate miR-96 expression is required for mouse retinal homeostasis.
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| http://dx.doi.org/10.1016/j.bbrc.2024.150048 | DOI Listing |
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