PIN1 protects auditory hair cells from senescence via autophagy

Background Age-related hearing loss is an increasing sensorineural hearing loss. But the pathogenesis of ARHL has not been clarified. Herein, we studied the role and significance of PIN1 in regulating autophagy activity in senescence HEI-OC1cells and HCs. Methods and Results C57BL/6 mice and HEI-OC1...

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Main Authors: Zhe Lv, Yanzhuo Zhang, Huan Cao, Qingjuan Liu, Xiaojuan Feng, Huan Yin, BaoShan Wang
Format: Article
Language:English
Published: PeerJ Inc. 2022-11-01
Series:PeerJ
Subjects:
Online Access:https://peerj.com/articles/14267.pdf
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author Zhe Lv
Yanzhuo Zhang
Huan Cao
Qingjuan Liu
Xiaojuan Feng
Huan Yin
BaoShan Wang
author_facet Zhe Lv
Yanzhuo Zhang
Huan Cao
Qingjuan Liu
Xiaojuan Feng
Huan Yin
BaoShan Wang
author_sort Zhe Lv
collection DOAJ
description Background Age-related hearing loss is an increasing sensorineural hearing loss. But the pathogenesis of ARHL has not been clarified. Herein, we studied the role and significance of PIN1 in regulating autophagy activity in senescence HEI-OC1cells and HCs. Methods and Results C57BL/6 mice and HEI-OC1 cells were contained in our research. Transfection of plasmids and juglone were used to upregulate or inhibit the PIN 1 expression. Immunofluorescence and Western blot were used to detect the expression of PIN1, LC3, p62, p21 and p16 protein levels in the hair cells of C57BL/6 mice cochleae and HEI-OC1 cells. Senescence-associated β-galactosidase (SA-β-gal) staining was used to investigate the senescent level.The results of this study showed that the level of autophagy increased in the senescent auditory hair cells. When inhibited the autophagy level with 3-MA, the senescent HEI-OC1 cells were alleviated. The autophagy activity in senescent HEI-OC1 cells also could be reduced by overexpressing PIN1 protein. On the contrary, inhibiting PIN1 could increase the autophagy level of senescent cells and cochlear hair cells. Conclusion PIN1 might regulate autophagy activity to induce the senescent of HEI-OC1cells and HCs, which will provide a theoretical support for the prevention and treatment of age-related hearing loss.
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spelling doaj.art-599069dfcd9e4828b9537356c23f3d762023-12-03T06:53:48ZengPeerJ Inc.PeerJ2167-83592022-11-0110e1426710.7717/peerj.14267PIN1 protects auditory hair cells from senescence via autophagyZhe Lv0Yanzhuo Zhang1Huan Cao2Qingjuan Liu3Xiaojuan Feng4Huan Yin5BaoShan Wang6Department of Otorhinolaryngology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, ChinaDepartment of Otorhinolaryngology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, ChinaDepartment of Otorhinolaryngology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, ChinaDepartment of Pathology, Hebei Key Laboratory of Nephrology, Center of Metabolic Diseases and Cancer Research, Hebei Medical University, Shijiazhuang, Hebei, ChinaDepartment of Pathology, Hebei Key Laboratory of Nephrology, Center of Metabolic Diseases and Cancer Research, Hebei Medical University, Shijiazhuang, Hebei, ChinaDepartment of Otorhinolaryngology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, ChinaDepartment of Otorhinolaryngology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, ChinaBackground Age-related hearing loss is an increasing sensorineural hearing loss. But the pathogenesis of ARHL has not been clarified. Herein, we studied the role and significance of PIN1 in regulating autophagy activity in senescence HEI-OC1cells and HCs. Methods and Results C57BL/6 mice and HEI-OC1 cells were contained in our research. Transfection of plasmids and juglone were used to upregulate or inhibit the PIN 1 expression. Immunofluorescence and Western blot were used to detect the expression of PIN1, LC3, p62, p21 and p16 protein levels in the hair cells of C57BL/6 mice cochleae and HEI-OC1 cells. Senescence-associated β-galactosidase (SA-β-gal) staining was used to investigate the senescent level.The results of this study showed that the level of autophagy increased in the senescent auditory hair cells. When inhibited the autophagy level with 3-MA, the senescent HEI-OC1 cells were alleviated. The autophagy activity in senescent HEI-OC1 cells also could be reduced by overexpressing PIN1 protein. On the contrary, inhibiting PIN1 could increase the autophagy level of senescent cells and cochlear hair cells. Conclusion PIN1 might regulate autophagy activity to induce the senescent of HEI-OC1cells and HCs, which will provide a theoretical support for the prevention and treatment of age-related hearing loss.https://peerj.com/articles/14267.pdfARHLHEI-OC1 cellsPIN1AutophagySenescence
spellingShingle Zhe Lv
Yanzhuo Zhang
Huan Cao
Qingjuan Liu
Xiaojuan Feng
Huan Yin
BaoShan Wang
PIN1 protects auditory hair cells from senescence via autophagy
PeerJ
ARHL
HEI-OC1 cells
PIN1
Autophagy
Senescence
title PIN1 protects auditory hair cells from senescence via autophagy
title_full PIN1 protects auditory hair cells from senescence via autophagy
title_fullStr PIN1 protects auditory hair cells from senescence via autophagy
title_full_unstemmed PIN1 protects auditory hair cells from senescence via autophagy
title_short PIN1 protects auditory hair cells from senescence via autophagy
title_sort pin1 protects auditory hair cells from senescence via autophagy
topic ARHL
HEI-OC1 cells
PIN1
Autophagy
Senescence
url https://peerj.com/articles/14267.pdf
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AT yanzhuozhang pin1protectsauditoryhaircellsfromsenescenceviaautophagy
AT huancao pin1protectsauditoryhaircellsfromsenescenceviaautophagy
AT qingjuanliu pin1protectsauditoryhaircellsfromsenescenceviaautophagy
AT xiaojuanfeng pin1protectsauditoryhaircellsfromsenescenceviaautophagy
AT huanyin pin1protectsauditoryhaircellsfromsenescenceviaautophagy
AT baoshanwang pin1protectsauditoryhaircellsfromsenescenceviaautophagy