Disturbance in the protein landscape of cochlear perilymph in an Alzheimer’s disease mouse model

Fukuda M., Okanishi H., Ino D., et al. (2024) Disturbance in the protein landscape of cochlear perilymph in an Alzheimer’s disease mouse model. PLoS ONE 19, e0303375. https://doi.org/10.1371/journal.pone.0303375.Hearing loss is a pivotal risk factor for dementia. It has recently emerged that a disruption in the intercommunication between the cochlea and brain is a key process in the initiation and progression of this disease. However, whether the cochlear properties can be influenced by pathological signals associated with dementia remains unclear. In this study, using a mouse model of Alzheimer’s disease (AD), we investigated the impacts of the AD-like amyloid β (Aβ) pathology in the brain on the cochlea. Despite little detectable change in the age-related shift of the hearing threshold, we observed quantitative and qualitative alterations in the protein profile in perilymph, an extracellular fluid that fills the path of sound waves in the cochlea. Our findings highlight the potential contribution of Aβ pathology in the brain to the disturbance of cochlear homeostasis

The effect of corneal epithelial cells on the collagen gel contraction by keratocytes

Abstract: To understand the mechanism of the contraction of cicatricial tissues after corneal stromal wounding, we investigated the effect of corneal epithelial cells on the collagen gel contraction by keratocytes. Subcultured rabbit keratocytes were embedded in type I collagen gel and cultured. Rabbit corneal epithelial cells were cultured separately and the culture medium was collected and used as an epithelial cell-conditioned medium (ECCM). The collagen gel contraction by keratocytes was determined by measuring the diameters of the collagen disks once a day for 5 days. In the presence of fetal calf serum, the diameter of the collagen gel decreased in linear proportion to the number of keratocytes, but in inverse proportion to the concentration of collagen. The addition of the ECCM enhanced the collagen gel contraction by keratocytes in a dose-dependent manner. This stimulatory activity was found in the ECCM obtained from 3-to 7-day cultures of epithelial cells. These findings suggest that corneal epithelial cells secrete factor(s) that stimulate the collagen gel contraction by keratocytes. Jpn J Ophthalmol 1998;42:174-17