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Updated: Feb 26, 2026
Spinal Cord Neurons Isolation and Culture from Neonatal Mice
Published on: July 11, 2017
Spinal cord ischemia-reperfusion causes damage of neurocyte by inhibiting RAP2C
Yong Qiao1, Changliang Peng1, Ji Li1
1a Department of Spinal Surgery , The Second Hospital of Shandong University , Ji'nan , China.
Objective:
To explore the mechanism of RAP2C participating in spinal cord ischemia-reperfusion injury (SCII).
Materials And Methods:
mRNA expressions of miR-204 and RAP2C were measured by qRT-PCR. Protein level of RAP2C was detected by Western blot. Cell apoptosis in AGE1.HN and PC12 cells was detected by Annexin V/propidium iodide assay. The effect of miR-204 knockdown or overexpression on RAP2C expression was observed by luciferase assay.
Results:
In this experimental research, RAP2C expression in SCII group was lower than control group, while miR-204 expression was higher. In addition, RAP2C expression in AGE1.HN and PC12 cells under hypoxic condition was lower than control group, while miR-204 expression was higher. Hypoxia increased cell apoptosis, and overexpression of RAP2C reversed this effect. In cells treated with hypoxia and miRNA-204 inhibitor, hypoxia upregulated the expression of miR-204, while miRNA-204 inhibitor reversed this effect. Hypoxia downregulated the expression of RAP2C, while miR-204 inhibitor reversed this effect. Moreover, miR-204 could bind to 3'-UTR of RAP2C. And miR-204 inhibitor upregulated the activity and expression of RAP2C, while miR-204 mimic played the opposite role. Finally, hypoxia downregulated RAP2C expression, miR-204 inhibitor upregulated RAP2C expression, while Ad-sh-RAP2C inhibited RAP2C expression. What's more, hypoxia increased the apoptosis rate, miR-204 inhibitor decreased the apoptosis rate, while si-RAP2C increased the apoptosis rate.
Conclusion:
SCII causes increase of neurocyte apoptosis by inhibiting RAP2C via miR-204.
