Published online Feb 28, 2012. doi: 10.5319/wjo.v2.i1.1
Revised: November 2, 2011
Accepted: February 27, 2012
Published online: February 28, 2012
AIM: To study the effects of adeno-associated virus (AAV) delivered short hairpin RNAs (shRNAs) on adult CD-1 mouse cochlea damaged by aminoglycoside antibiotic kanamycin.
METHODS: Three different shRNAs were designed (p27 Kip1, p53 and p27 Kip1+p53) and tested in COS cells. A total of 20 adult CD-1 mice were used in the experiment. Mice were divided into five different groups (four animals/group) depending on the AAV-shRNA construct they received and whether they received kanamycin or not. Saline and AAV-EGFP injected animals were used as controls. All constructs were injected through the round window membrane (RWM) into the cochlea. Cochleae were harvested after 1 mo. Apoptosis was detected with Tunel labeling from paraffin-embedded cochlear tissue sections.
RESULTS: AAV2/2-p27 Kip1-shRNA and AAV2/2-p53-shRNA were tested in COS cells. Western blotting analysis confirmed that both constructs silenced their target genes effectively in the cell culture. AAV2/2-shRNA constructs were injected into the cochlea of CD-1 mice through the intact RWM. Cotransduction of individual AAV2/2-shRNAs with AAV2/2-EGFP resulted in EGFP expression in the organ of Corti. Kanamycin treatment had no effect on the expression pattern of the EGFP. AAV2/2-shRNA treated mice (either with p53 or p27Kip1and p53 together) showed fewer apoptotic hair cells in the cochlea than the control group (P < 0.05; AAV2/2-p53-shRNA vs saline P = 0.00014; AAV2/2-p27+p53-shRNA vs saline P = 0.0011). AAV2/2-p27-shRNA injected cochleae showed no significant difference in the number of apoptotic cells when compared to the saline injected cochleae.
CONCLUSION: Silencing of p53 protein in the kanamycin treated ears may decrease cell death in the organ of Corti.