98%
921
2 minutes
20
Objective: Screen for differential proteins in the cochlea of mice associated with Age-Related Hearing Loss (ARHL), analyze and validate the expression of specific differential proteins and genes in the cochlea and auditory cortex of ARHL mice, and preliminarily explore their potential mechanisms of action.
Methods: ABR (Auditory Brainstem Response) hearing tests were conducted to select 15-month-old C57BL/6 mice with significantly decreased hearing as the experimental group and 2-month-old mice with normal hearing as the control group. Cochleae were dissected, and unlabeled quantitative proteomics was employed to identify and analyze differentially expressed proteins in the inner ear of the two groups of mice. Key node proteins were selected via the STRING database and Cytoscape analysis. The expression of two selected proteins, ApoE and Spp1, in the cochlea was detected using qRT-PCR, Western blot, and immunofluorescence techniques, and their expression in the auditory cortex of the brain was further explored.
Results: Label-free quantitative proteomics identified 115 differentially expressed proteins in the cochlea of 15-month-old ARHL mice compared to 2-month-old hearing-normal mice, including 42 upregulated and 73 downregulated proteins. GO and KEGG enrichment analyses revealed significant enrichment of differentially expressed proteins in functions and signaling pathways associated with neurodegenerative diseases and neurotransmission. Protein-Protein Interaction (PPI) analysis using the STRING database and Cytoscape selection identified ApoE and Spp1 as key hub proteins. Validation via qRT-PCR, Western blot, and immunofluorescence demonstrated that both ApoE and Spp1 were highly expressed in the cochlea and auditory cortex of the ARHL mice compare to 2-month-old hearing-normal mice.
Conclusion: ApoE and Spp1 are upregulated in the cochlea of ARHL mice, particularly in spiral ganglion neurons, and in the auditory cortex, suggesting their potential involvement in the pathogenesis and progression of ARHL through the modulation of auditory neural conduction systems.
Level Of Evidence: Level 2.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC12274660 | PMC |
http://dx.doi.org/10.1016/j.bjorl.2025.101674 | DOI Listing |
J Exp Med
November 2025
Institute of Molecular Medicine, Feinstein Institutes for Medical Research, Manhasset, NY, USA.
Monocytes and macrophages in patients with lupus nephritis exhibit altered behavior compared with healthy kidneys. How to optimally use mouse models to develop treatments targeting these cells is poorly understood. This study compared intrarenal myeloid cells in four mouse models and 155 lupus nephritis patients using single-cell profiling, spatial transcriptomics, and functional studies.
View Article and Find Full Text PDFBraz J Otorhinolaryngol
July 2025
Shandong Provincial Hospital Affiliated to Shandong First Medical University, Department of Pathology, Shandong, China. Electronic address:
Objective: Screen for differential proteins in the cochlea of mice associated with Age-Related Hearing Loss (ARHL), analyze and validate the expression of specific differential proteins and genes in the cochlea and auditory cortex of ARHL mice, and preliminarily explore their potential mechanisms of action.
Methods: ABR (Auditory Brainstem Response) hearing tests were conducted to select 15-month-old C57BL/6 mice with significantly decreased hearing as the experimental group and 2-month-old mice with normal hearing as the control group. Cochleae were dissected, and unlabeled quantitative proteomics was employed to identify and analyze differentially expressed proteins in the inner ear of the two groups of mice.
Mamm Genome
September 2025
Department of Cardiology, The First Affiliated Hospital of Guangxi Medical University, Nanning, China.
This study aims to characterize B cell subtypes in mice following myocardial infarction (MI) and identify potential therapeutic targets for adverse remodeling post-MI. The scRNA-seq (GSE163129) and bulk RNA sequencing data (GSE19322) of mice post-MI were obtained from the GEO database. Seurat, gene set enrichment analysis, SCENIC analysis, Monocle 2 and NichNet analysis were performed in scRNA-seq data.
View Article and Find Full Text PDFThe host retinal microglia and macrophage activation remains a major challenge for the integration of donor neurons following transplantation. Previously, we and others have shown that it is possible to increase donor retinal ganglion cell (RGC) survival by inhibiting the microglia-RGC interaction with Annexin V or through reprogramming microglia with the soluble Fas ligand. However, the exact mechanisms of the microglia/macrophage activation and their heterogeneity following transplantation remain unknown.
View Article and Find Full Text PDFCell Rep
June 2025
Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA. Electronic address:
Advancements in human induced pluripotent stem cell (hiPSC) technology have enabled co-culture models for disease modeling in physiologically relevant systems. However, co-culturing protocols face challenges in usability and consistency. Here, we introduce a robust, reproducible hiPSC-derived co-culture system integrating astrocytes, neurons, and microglia.
View Article and Find Full Text PDF