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Published on: July 14, 2016
MiR-93-5p inhibits retinal neurons apoptosis by regulating PDCD4 in acute ocular hypertension model
Cheng Tan1,2, Wenjia Shi1, Yun Zhang1
1Department of Human Anatomy and Neurobiology, School of Basic Medical Sciences, Central South University, Changsha, China.
Abstract:
The present study focused on the effect of miR-93-5p on apoptosis of retinal neurons in acute ocular hypertension (AOH) model by regulating PDCD4 and explored its related mechanism. We detected that miR-93-5p expression was decreased and PDCD4 expression was increased in the AOH retina by qRT-PCR. Therefore, we explored the role of miR-93-5p and PDCD4. MiR-93-5p overexpression inhibited the apoptosis of retinal neurons and the expression of PDCD4 in vivo and in vitro. Inhibiting the expression of PDCD4 via transfected interfering RNA decreased the apoptosis of retinal cells and increased the expression of PI3K/Akt pathway-related proteins in vitro. However, the addition of PI3K protein inhibitor LY294002 reversed this effect, leading to a decrease of PI3K/Akt pathway protein expression and an increase of apoptosis-related protein Bax/Bcl-2 expression ratio. Finally, up-regulating miR-93-5p or down-regulating PDCD4 increased the expression of PI3K/Akt pathway protein in vivo. In conclusion, under the condition of AOH injury, miR-93-5p-inhibiting PDCD4 expression reduced the apoptosis of retinal neurons by activating PI3K/Akt pathway.
Insights
MicroRNA-93-5p (miR-93-5p) protects retinal neurons from acute ocular hypertension (AOH) by downregulating PDCD4. This mechanism activates the PI3K/Akt pathway, reducing neuronal apoptosis.
Area of Science:
- Ophthalmology
- Molecular Biology
- Neuroscience
Background:
- Acute ocular hypertension (AOH) can lead to retinal neuron apoptosis.
- The role of microRNAs, specifically miR-93-5p, in AOH-induced retinal damage is not fully understood.
- PDCD4 is implicated in apoptosis, but its specific role in AOH requires further investigation.
Purpose of the Study:
- To investigate the effect of miR-93-5p on retinal neuron apoptosis in an AOH model.
- To explore the regulatory relationship between miR-93-5p and PDCD4 in this context.
- To elucidate the underlying molecular mechanism involving the PI3K/Akt pathway.
Main Methods:
- Quantitative real-time PCR (qRT-PCR) to measure miR-93-5p and PDCD4 expression.
- In vivo and in vitro experiments involving miR-93-5p overexpression and PDCD4 inhibition (using interfering RNA).
- Assessment of retinal neuron apoptosis and expression of PI3K/Akt pathway proteins.
- Pharmacological inhibition of the PI3K/Akt pathway using LY294002.
Main Results:
- miR-93-5p expression was decreased, while PDCD4 expression was increased in the AOH retina.
- Overexpression of miR-93-5p inhibited retinal neuron apoptosis and PDCD4 expression.
- Inhibition of PDCD4 reduced apoptosis and enhanced PI3K/Akt pathway protein expression.
- LY294002 treatment reversed these effects, increasing apoptosis and altering the Bax/Bcl-2 ratio.
- Upregulating miR-93-5p or downregulating PDCD4 activated the PI3K/Akt pathway in vivo.
Conclusions:
- miR-93-5p plays a protective role against AOH-induced retinal neuron apoptosis.
- miR-93-5p exerts its protective effect by inhibiting PDCD4 expression.
- The miR-93-5p/PDCD4 axis activates the PI3K/Akt pathway, thereby reducing retinal neuron apoptosis in AOH.
