Identification and Characterization of mRNA and lncRNA Expression Profiles in Age-Related Hearing Loss
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Objectives. Age-related hearing loss (ARHL), or presbycusis, is caused by disorders of sensory hair cells and auditory neu-rons. Many studies have suggested that the accumulation of mitochondrial DNA damage, the production of reactiveoxygen species, noise, inflammation, and decreased antioxidant function are associated with subsequent cochlear se-nescence in response to aging stress. Long non-coding RNA (lncRNA) has been reported to play important roles invarious diseases. However, the function of lncRNA in ARHL remains unclear. In this study, we analyzed the commonexpression profiles of messenger RNA (mRNA) and lncRNA through ARHL-related RNA-sequencing datasets. Methods. We selected and downloaded three different sets of RNA-sequencing data for ARHL. We performed differentialexpression analysis to find common mRNA and lncRNA profiles in the cochleae of aged mice compared to youngmice. Gene Ontology (GO) analysis was used for functional exploration. Real-time quantitative reverse-transcriptionpolymerase chain reaction (qRT-PCR) was performed to validate mRNAs and lncRNAs. In addition, we performedtrans target prediction analysis with differentially expressed mRNAs and lncRNAs to understand the function ofthese mRNAs and lncRNAs in ARHL. Results. We identified 112 common mRNAs and 10 common lncRNAs in the cochleae of aged mice compared to youngmice. GO analysis showed that the 112 upregulated mRNAs were enriched in the defense response pathway. Whenwe performed qRT-PCR with 1 mM H2O2-treated House Ear Institute-Organ of Corti 1 (HEI-OC1) cells, the qRT-PCR results were consistent with the RNA-sequencing analysis data. lncRNA-mRNA networks were constructed us-ing the 10 common lncRNAs and 112 common mRNAs in ARHL. Conclusion. Our study provides a comprehensive understanding of the common mRNA and lncRNA expression profiles inARHL. Knowledge of ARHL-associated mRNAs and lncRNAs could be useful for better understanding ARHL andthese mRNAs and lncRNAs might be a potential therapeutic target for preventing ARHL.
Abstract
Objectives. Age-related hearing loss (ARHL), or presbycusis, is caused by disorders of sensory hair cells and auditory neu-rons. Many studies have suggested that the accumulation of mitochondrial DNA damage, the production of reactiveoxygen species, noise, inflammation, and decreased antioxidant function are associated with subsequent cochlear se-nescence in response to aging stress. Long non-coding RNA (lncRNA) has been reported to play important roles invarious diseases. However, the function of lncRNA in ARHL remains unclear. In this study, we analyzed the commonexpression profiles of messenger RNA (mRNA) and lncRNA through ARHL-related RNA-sequencing datasets. Methods. We selected and downloaded three different sets of RNA-sequencing data for ARHL. We performed differentialexpression analysis to find common mRNA and lncRNA profiles in the cochleae of aged mice compared to youngmice. Gene Ontology (GO) analysis was used for functional exploration. Real-time quantitative reverse-transcriptionpolymerase chain reaction (qRT-PCR) was performed to validate mRNAs and lncRNAs. In addition, we performedtrans target prediction analysis with differentially expressed mRNAs and lncRNAs to understand the function ofthese mRNAs and lncRNAs in ARHL. Results. We identified 112 common mRNAs and 10 common lncRNAs in the cochleae of aged mice compared to youngmice. GO analysis showed that the 112 upregulated mRNAs were enriched in the defense response pathway. Whenwe performed qRT-PCR with 1 mM H2O2-treated House Ear Institute-Organ of Corti 1 (HEI-OC1) cells, the qRT-PCR results were consistent with the RNA-sequencing analysis data. lncRNA-mRNA networks were constructed us-ing the 10 common lncRNAs and 112 common mRNAs in ARHL. Conclusion. Our study provides a comprehensive understanding of the common mRNA and lncRNA expression profiles inARHL. Knowledge of ARHL-associated mRNAs and lncRNAs could be useful for better understanding ARHL andthese mRNAs and lncRNAs might be a potential therapeutic target for preventing ARHL.
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