Deletion of Kcnj16 in Mice Does Not Alter Auditory Function
Endolymphatic potential (EP) is the main driving force behind the sensory transduction of hearing, and K+ is the main charge carrier. Kir5.1 is a K+ transporter that plays a significant role in maintaining EP homeostasis, but the expression pattern and role of Kir5.1 (which is encoded by the Kcnj16...
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Frontiers Media S.A.
2021-02-01
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| Series: | Frontiers in Cell and Developmental Biology |
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| Online Access: | https://www.frontiersin.org/articles/10.3389/fcell.2021.630361/full |
| _version_ | 1819050498527854592 |
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| author | Jun Lv Xiaolong Fu Yige Li Guodong Hong Peipei Li Jing Lin Youfang Xun Youfang Xun Lucheng Fang Weibin Weng Rongyu Yue Geng-Lin Li Bing Guan He Li Yideng Huang Yideng Huang Renjie Chai Renjie Chai Renjie Chai Renjie Chai |
| author_facet | Jun Lv Xiaolong Fu Yige Li Guodong Hong Peipei Li Jing Lin Youfang Xun Youfang Xun Lucheng Fang Weibin Weng Rongyu Yue Geng-Lin Li Bing Guan He Li Yideng Huang Yideng Huang Renjie Chai Renjie Chai Renjie Chai Renjie Chai |
| author_sort | Jun Lv |
| collection | DOAJ |
| description | Endolymphatic potential (EP) is the main driving force behind the sensory transduction of hearing, and K+ is the main charge carrier. Kir5.1 is a K+ transporter that plays a significant role in maintaining EP homeostasis, but the expression pattern and role of Kir5.1 (which is encoded by the Kcnj16 gene) in the mouse auditory system has remained unclear. In this study, we found that Kir5.1 was expressed in the mouse cochlea. We checked the inner ear morphology and measured auditory function in Kcnj16–/– mice and found that loss of Kcnj16 did not appear to affect the development of hair cells. There was no significant difference in auditory function between Kcnj16–/– mice and wild-type littermates, although the expression of Kcnma1, Kcnq4, and Kcne1 were significantly decreased in the Kcnj16–/– mice. Additionally, no significant differences were found in the number or distribution of ribbon synapses between the Kcnj16–/– and wild-type mice. In summary, our results suggest that the Kcnj16 gene is not essential for auditory function in mice. |
| first_indexed | 2024-12-21T11:49:00Z |
| format | Article |
| id | doaj.art-94714c1b248c456fbbc05cf8e7d9377d |
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| issn | 2296-634X |
| language | English |
| last_indexed | 2024-12-21T11:49:00Z |
| publishDate | 2021-02-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Cell and Developmental Biology |
| spelling | doaj.art-94714c1b248c456fbbc05cf8e7d9377d2022-12-21T19:05:07ZengFrontiers Media S.A.Frontiers in Cell and Developmental Biology2296-634X2021-02-01910.3389/fcell.2021.630361630361Deletion of Kcnj16 in Mice Does Not Alter Auditory FunctionJun Lv0Xiaolong Fu1Yige Li2Guodong Hong3Peipei Li4Jing Lin5Youfang Xun6Youfang Xun7Lucheng Fang8Weibin Weng9Rongyu Yue10Geng-Lin Li11Bing Guan12He Li13Yideng Huang14Yideng Huang15Renjie Chai16Renjie Chai17Renjie Chai18Renjie Chai19Department of Otolaryngology-Head and Neck Surgery, First Affiliated Hospital of Wenzhou Medical University, Wenzhou, ChinaState Key Laboratory of Bioelectronics, School of Life Sciences and Technology, Jiangsu Province High-Tech Key Laboratory for Bio-Medical Research, Southeast University, Nanjing, ChinaState Key Laboratory of Bioelectronics, School of Life Sciences and Technology, Jiangsu Province High-Tech Key Laboratory for Bio-Medical Research, Southeast University, Nanjing, ChinaState Key Laboratory of Bioelectronics, School of Life Sciences and Technology, Jiangsu Province High-Tech Key Laboratory for Bio-Medical Research, Southeast University, Nanjing, ChinaSchool of Life Sciences and Key Laboratory of the Ministry of Education for Experimental Teratology, Shandong University, Jinan, ChinaWaksman Institute, Rutgers, The State University of New Jersey, Piscataway, NJ, United StatesDepartment of Otolaryngology, Head and Neck Surgery, Xiangya School of Medicine, Central South University, Changsha, ChinaDepartment of Otolaryngology, Head and Neck Surgery, Clinical Medical College of Yangzhou University, Yangzhou, ChinaDepartment of Otolaryngology-Head and Neck Surgery, First Affiliated Hospital of Wenzhou Medical University, Wenzhou, ChinaDepartment of Otolaryngology-Head and Neck Surgery, First Affiliated Hospital of Wenzhou Medical University, Wenzhou, ChinaDepartment of Otolaryngology-Head and Neck Surgery, Provincial Hospital Affiliated to Shandong University, Jinan, ChinaDepartment of Otorhinolaryngology and ENT Institute, Eye and ENT Hospital, Fudan University, Shanghai, ChinaDepartment of Otolaryngology, Head and Neck Surgery, Clinical Medical College of Yangzhou University, Yangzhou, ChinaDepartment of Otolaryngology-Head and Neck Surgery, First Affiliated Hospital of Wenzhou Medical University, Wenzhou, ChinaDepartment of Otolaryngology-Head and Neck Surgery, First Affiliated Hospital of Wenzhou Medical University, Wenzhou, ChinaDepartment of Otolaryngology-Head and Neck Surgery, Hwa Mei Hospital, University of Chinese Academy of Sciences, Ningbo, ChinaDepartment of Otolaryngology-Head and Neck Surgery, First Affiliated Hospital of Wenzhou Medical University, Wenzhou, ChinaState Key Laboratory of Bioelectronics, School of Life Sciences and Technology, Jiangsu Province High-Tech Key Laboratory for Bio-Medical Research, Southeast University, Nanjing, China0Co-Innovation Center of Neuroregeneration, Nantong University, Nantong, China1Institute for Stem Cell and Regeneration, Chinese Academy of Sciences, Beijing, ChinaEndolymphatic potential (EP) is the main driving force behind the sensory transduction of hearing, and K+ is the main charge carrier. Kir5.1 is a K+ transporter that plays a significant role in maintaining EP homeostasis, but the expression pattern and role of Kir5.1 (which is encoded by the Kcnj16 gene) in the mouse auditory system has remained unclear. In this study, we found that Kir5.1 was expressed in the mouse cochlea. We checked the inner ear morphology and measured auditory function in Kcnj16–/– mice and found that loss of Kcnj16 did not appear to affect the development of hair cells. There was no significant difference in auditory function between Kcnj16–/– mice and wild-type littermates, although the expression of Kcnma1, Kcnq4, and Kcne1 were significantly decreased in the Kcnj16–/– mice. Additionally, no significant differences were found in the number or distribution of ribbon synapses between the Kcnj16–/– and wild-type mice. In summary, our results suggest that the Kcnj16 gene is not essential for auditory function in mice.https://www.frontiersin.org/articles/10.3389/fcell.2021.630361/fullKir5.1hair cellendolymphatic potentialcochleahearing loss |
| spellingShingle | Jun Lv Xiaolong Fu Yige Li Guodong Hong Peipei Li Jing Lin Youfang Xun Youfang Xun Lucheng Fang Weibin Weng Rongyu Yue Geng-Lin Li Bing Guan He Li Yideng Huang Yideng Huang Renjie Chai Renjie Chai Renjie Chai Renjie Chai Deletion of Kcnj16 in Mice Does Not Alter Auditory Function Frontiers in Cell and Developmental Biology Kir5.1 hair cell endolymphatic potential cochlea hearing loss |
| title | Deletion of Kcnj16 in Mice Does Not Alter Auditory Function |
| title_full | Deletion of Kcnj16 in Mice Does Not Alter Auditory Function |
| title_fullStr | Deletion of Kcnj16 in Mice Does Not Alter Auditory Function |
| title_full_unstemmed | Deletion of Kcnj16 in Mice Does Not Alter Auditory Function |
| title_short | Deletion of Kcnj16 in Mice Does Not Alter Auditory Function |
| title_sort | deletion of kcnj16 in mice does not alter auditory function |
| topic | Kir5.1 hair cell endolymphatic potential cochlea hearing loss |
| url | https://www.frontiersin.org/articles/10.3389/fcell.2021.630361/full |
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