Auditory hair cell damage induced by aminoglycoside antibiotics (AmAn) leads to hearing loss, which has a serious effect on people's mental and physical health. This ototoxicity is thought to be related with the excessive accumulation of reactive oxygen species (ROS) in hair cells. However, therapeutic agents that protect hair cells are limited. Marine peptides have been shown to have excellent potential applications in disease prevention and treatment. Therefore, this study investigated the protective effects of an active peptide from against AmAn-induced hair cell damage using the model of hair cell damage zebrafish. We identified the number, ultrastructure, and function of hair cells using fluorescence probes and scanning electron microscopy. The uptake of AmAn, ROS level, mitochondrial permeability transition pore, and apoptosis in hair cells were also tested by fluorescence labeling and TUNEL assay. The molecular mechanism for hair cell protection exerted by the peptide was detected by a real-time quantitative PCR assay. The results indicated that the peptide suppressed the uptake of AmAn but did not damage the function of hair cells mediating hearing. It also prevented ROS accumulation, decreased the occurrence of apoptosis, and rescued the abnormal opening and expressions of mitochondrial permeability transition pore and genes related to antioxidants. The peptide may be an effective therapeutic agent for AmAn-induced ototoxicity. In the future, we plan to use mammalian models to further investigate the otoprotective effect of the peptide.
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http://dx.doi.org/10.3390/md22110519 | DOI Listing |
Bio Protoc
January 2025
ENT Institute and Department of Otorhinolaryngology, Eye & ENT Hospital, Fudan University, Shanghai, China.
The organ of Corti, located in the inner ear, is the primary organ responsible for animal hearing. Each hair cell has a V-shaped or U-shaped hair bundle composed of actin-filled stereocilia and a kinocilium supported by true transport microtubules. Damage to these structures due to noise exposure, drug toxicity, aging, or environmental factors can lead to hearing loss and other disorders.
View Article and Find Full Text PDFAdv Sci (Weinh)
January 2025
Department of Otolaryngology, Case Western Reserve University, Cleveland, OH, 44106, USA.
Usher syndrome type 1C (USH1C) is a genetic disorder caused by mutations in the USH1C gene, which encodes harmonin, a key component of the mechanoelectrical transduction complex in auditory and vestibular hair cells. USH1C leads to deafness and vestibular dysfunction in humans. An Ush1c knockout (KO) mouse model displaying these characteristic deficits is generated in our laboratory.
View Article and Find Full Text PDFHear Res
January 2025
Columbia University Irving Medical Center, Department of Otolaryngology, Head and Neck Surgery, 180 Fort Washington Ave, New York, 10032, NY, USA; Columbia University, Department of Biomedical Engineering, 1210 Amsterdam Ave, New York, 10027, NY, USA.
Sound-evoked displacement responses at the outer hair cell-Deiters' cell junction (OHC-DC) are of significant interest in cochlear mechanics, as OHCs are believed to be in part responsible for active tuning enhancement and amplification. Motion in the cochlea is three-dimensional, and the architecture of the organ of Corti complex (OCC) suggests the presence and mechanical importance of all three components of motion. Optical coherence tomography (OCT) displacement measurements of OHC-DC motion from different experimental preparations often show disparate results, potentially due to OCT measuring only the motion component along the beam axis.
View Article and Find Full Text PDFPlant Cell Physiol
January 2025
Institute for Chemical Research, Kyoto University, Gokasho, Uji, 611-0011 Kyoto, Japan.
Lotus japonicus-ROOT HAIR LESS1-LIKE1 (LRL1) of Arabidopsis thaliana encodes a basic helix-loop-helix (bHLH) transcription factor (TF) involved in root hair development. Root hair development is regulated by an elaborate transcriptional network, in which GLABRA2 (GL2), a key negative regulator, directly represses bHLH TF genes, including LRL1 and ROOT HAIR DEFECTIVE6 (RHD6). Although RHD6 and its paralogous TFs have been shown to connect downstream to genes involved in cell morphological events such as endomembrane and cell wall modification, the network downstream of LRL1 remains elusive.
View Article and Find Full Text PDFJ Dermatol
January 2025
Department of Dermatology, Tohoku University Graduate School of Medicine, Sendai, Miyagi, Japan.
Alopecia areata (AA) is a chronic, autoimmune skin disease characterized by non-scarring hair loss. Baricitinib, a Janus kinase inhibitor (JAKi), prevents hair loss and promotes hair regrowth by inhibiting the inflammatory Janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling pathway involved in cytotoxic T cell responses targeting hair follicles. The introduction of JAKi has transformed treatment against severe AA.
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