A Novel Animal Model of Hearing Loss Caused by Acute Endoplasmic Reticulum Stress in the Cochlea
Many stimuli such as ischemia, hypoxia, heat shock, amino acid starvation, and gene mutation, exhibit a cellular response called endoplasmic reticulum (ER) stress. ER stress induces expression of a series of genes, leading to cell survival or apoptosis. Previously, we found that in an animal model o...
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| Published in | Journal of Pharmacological Sciences Vol. 118; no. 3; pp. 363 - 372 |
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| Main Authors | , , , , |
| Format | Journal Article |
| Language | English |
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Japan
Elsevier B.V
2012
The Japanese Pharmacological Society Elsevier |
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| Abstract | Many stimuli such as ischemia, hypoxia, heat shock, amino acid starvation, and gene mutation, exhibit a cellular response called endoplasmic reticulum (ER) stress. ER stress induces expression of a series of genes, leading to cell survival or apoptosis. Previously, we found that in an animal model of hearing loss caused by acute mitochondrial dysfunction, several ER stress markers including C/EBP homologous protein were induced in the cochlear lateral wall. To elucidate the mechanism of hearing loss caused by ER stress, we established a novel animal model of hearing loss by perilymphatic perfusion of tunicamycin, an ER stress activator that inhibits N-acetylglucosamine transferases. Subacute and progressive hearing loss was observed at all sound frequencies studied, and stimulation of ER stress marker genes was noted in the cochlea. The outer hair cells were the most sensitive to ER stress in the cochlea. Electron microscopic analysis demonstrated degeneration of the subcellular organelles of the inner hair cells and nerve endings of the spiral ganglion cells. This newly established animal model of hearing loss from ER stress will provide additional insight into the mechanism of sensorineural hearing loss. |
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| AbstractList | 「Abstract. 」Many stimuli such as ischemia, hypoxia, heat shock, amino acid starvation, and gene mutation, exhibit a cellular response called endoplasmic reticulum (ER) stress. ER stress induces expression of a series of genes, leading to cell survival or apoptosis. Previously, we found that in an animal model of hearing loss caused by acute mitochondrial dysfunction, several ER stress markers including C/EBP homologous protein were induced in the cochlear lateral wall. To elucidate the mechanism of hearing loss caused by ER stress, we established a novel animal model of hearing loss by perilymphatic perfusion of tunicamycin, an ER stress activator that inhibits N-acetylglucosamine transferases. Subacute and progressive hearing loss was observed at all sound frequencies studied, and stimulation of ER stress marker genes was noted in the cochlea. The outer hair cells were the most sensitive to ER stress in the cochlea. Electron microscopic analysis demonstrated degeneration of the subcellular organelles of the inner hair cells and nerve endings of the spiral ganglion cells. This newly established animal model of hearing loss from ER stress will provide additional insight into the mechanism of sensorineural hearing loss. Many stimuli such as ischemia, hypoxia, heat shock, amino acid starvation, and gene mutation, exhibit a cellular response called endoplasmic reticulum (ER) stress. ER stress induces expression of a series of genes, leading to cell survival or apoptosis. Previously, we found that in an animal model of hearing loss caused by acute mitochondrial dysfunction, several ER stress markers including C/EBP homologous protein were induced in the cochlear lateral wall. To elucidate the mechanism of hearing loss caused by ER stress, we established a novel animal model of hearing loss by perilymphatic perfusion of tunicamycin, an ER stress activator that inhibits N-acetylglucosamine transferases. Subacute and progressive hearing loss was observed at all sound frequencies studied, and stimulation of ER stress marker genes was noted in the cochlea. The outer hair cells were the most sensitive to ER stress in the cochlea. Electron microscopic analysis demonstrated degeneration of the subcellular organelles of the inner hair cells and nerve endings of the spiral ganglion cells. This newly established animal model of hearing loss from ER stress will provide additional insight into the mechanism of sensorineural hearing loss. Many stimuli such as ischemia, hypoxia, heat shock, amino acid starvation, and gene mutation, exhibit a cellular response called endoplasmic reticulum (ER) stress. ER stress induces expression of a series of genes, leading to cell survival or apoptosis. Previously, we found that in an animal model of hearing loss caused by acute mitochondrial dysfunction, several ER stress markers including C/EBP homologous protein were induced in the cochlear lateral wall. To elucidate the mechanism of hearing loss caused by ER stress, we established a novel animal model of hearing loss by perilymphatic perfusion of tunicamycin, an ER stress activator that inhibits N-acetylglucosamine transferases. Subacute and progressive hearing loss was observed at all sound frequencies studied, and stimulation of ER stress marker genes was noted in the cochlea. The outer hair cells were the most sensitive to ER stress in the cochlea. Electron microscopic analysis demonstrated degeneration of the subcellular organelles of the inner hair cells and nerve endings of the spiral ganglion cells. This newly established animal model of hearing loss from ER stress will provide additional insight into the mechanism of sensorineural hearing loss. Keywords:: endoplasmic reticulum stress, tunicamycin, hearing loss, animal model |
| Author | Nakagawa, Susumu Matsunaga, Tatsuo Mizutari, Kunio Fujinami, Yoshiaki Mutai, Hideki |
| Author_xml | – sequence: 1 givenname: Yoshiaki surname: Fujinami fullname: Fujinami, Yoshiaki organization: Laboratory of Auditory Disorders, National Institute of Sensory Organs (NISO), National Tokyo Medical Center, 2-5-1 Higashigaoka, Meguro-ku, Tokyo 152-8902, Japan – sequence: 2 givenname: Hideki surname: Mutai fullname: Mutai, Hideki organization: Laboratory of Auditory Disorders, National Institute of Sensory Organs (NISO), National Tokyo Medical Center, 2-5-1 Higashigaoka, Meguro-ku, Tokyo 152-8902, Japan – sequence: 3 givenname: Kunio surname: Mizutari fullname: Mizutari, Kunio organization: Laboratory of Auditory Disorders, National Institute of Sensory Organs (NISO), National Tokyo Medical Center, 2-5-1 Higashigaoka, Meguro-ku, Tokyo 152-8902, Japan – sequence: 4 givenname: Susumu surname: Nakagawa fullname: Nakagawa, Susumu organization: Laboratory of Auditory Disorders, National Institute of Sensory Organs (NISO), National Tokyo Medical Center, 2-5-1 Higashigaoka, Meguro-ku, Tokyo 152-8902, Japan – sequence: 5 givenname: Tatsuo surname: Matsunaga fullname: Matsunaga, Tatsuo email: matsunagatatsuo@kankakuki.go.jp organization: Laboratory of Auditory Disorders, National Institute of Sensory Organs (NISO), National Tokyo Medical Center, 2-5-1 Higashigaoka, Meguro-ku, Tokyo 152-8902, Japan |
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| SubjectTerms | Activating Transcription Factor 4 - genetics animal model Animals Cochlea - pathology Cochlea - physiopathology Disease Models, Animal endoplasmic reticulum stress Endoplasmic Reticulum Stress - physiology Gene Expression Regulation hearing loss Hearing Loss - genetics Hearing Loss - pathology Hearing Loss - physiopathology Male Membrane Glycoproteins - genetics Rats Rats, Sprague-Dawley Transcription Factor CHOP - genetics tunicamycin Tunicamycin - administration & dosage |
| Title | A Novel Animal Model of Hearing Loss Caused by Acute Endoplasmic Reticulum Stress in the Cochlea |
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