Aldosterone inhibits Dot1l expression in guinea pig cochlea

Abstract Background Aldosterone relieves transcriptional repression of epithelial sodium channel (ENaC) by inhibiting Dot1a and Af9 expression and their interaction with ENaC promoter in various tissues. Expressions of ENaC and Af9 in inner ear have been identified. However, it is not known how Dot1...

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Main Authors: Shixun Zhong, Biyun Zhang, Li Qin, Qianying Wang, Xiaoli Luo
Format: Article
Language:English
Published: BMC 2023-01-01
Series:European Journal of Medical Research
Subjects:
Online Access:https://doi.org/10.1186/s40001-023-00994-y
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author Shixun Zhong
Biyun Zhang
Li Qin
Qianying Wang
Xiaoli Luo
author_facet Shixun Zhong
Biyun Zhang
Li Qin
Qianying Wang
Xiaoli Luo
author_sort Shixun Zhong
collection DOAJ
description Abstract Background Aldosterone relieves transcriptional repression of epithelial sodium channel (ENaC) by inhibiting Dot1a and Af9 expression and their interaction with ENaC promoter in various tissues. Expressions of ENaC and Af9 in inner ear have been identified. However, it is not known how Dot1l is regulated by aldosterone in inner ear. Methods Twenty-eight adult guinea pigs were randomly divided into the control group and treatment group. Aldosterone 1 mg/kg/d was injected intraperitoneally in the treatment group and saline in the control group for 7 days. Animals were killed 1 month later following auditory brainstem response examination. Histomorphology of cochlea was detected with hematoxylin–eosin staining, and Dot1l expression was examined with immunohistochemistry and Western blot. Results There was no significant difference in ABR thresholds before and after injection of aldosterone or saline in either group. Endolymphatic hydrops was found in 75% of animals in the treatment group. Dot1l was found in both groups in the stria vascularis, Reissner’s membrane, spiral limbus, organ of Corti and spiral ligament. Dot1l expression in the treatment group was decreased by aldosterone. Conclusions Dot1l in guinea pig cochlea is inhibited by aldosterone with induction of endolymphatic hydrops. Dot1l may be closely related to endolymph regulation by aldosterone and to pathogenesis of Meniere’s disease.
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spelling doaj.art-ecec38a015784938b8278f3d39983fbb2023-01-15T12:07:31ZengBMCEuropean Journal of Medical Research2047-783X2023-01-012811610.1186/s40001-023-00994-yAldosterone inhibits Dot1l expression in guinea pig cochleaShixun Zhong0Biyun Zhang1Li Qin2Qianying Wang3Xiaoli Luo4Department of Otolaryngology, The First Affiliated Hospital of Chongqing Medical UniversityDepartment of Otolaryngology, The First Affiliated Hospital of Chongqing Medical UniversityDepartment of Otolaryngology, Mianyang Central HospitalDepartment of Otolaryngology, The First Affiliated Hospital of Chongqing Medical UniversityDepartment of Otolaryngology, Chongqing Traditional Chinese Medicine HospitalAbstract Background Aldosterone relieves transcriptional repression of epithelial sodium channel (ENaC) by inhibiting Dot1a and Af9 expression and their interaction with ENaC promoter in various tissues. Expressions of ENaC and Af9 in inner ear have been identified. However, it is not known how Dot1l is regulated by aldosterone in inner ear. Methods Twenty-eight adult guinea pigs were randomly divided into the control group and treatment group. Aldosterone 1 mg/kg/d was injected intraperitoneally in the treatment group and saline in the control group for 7 days. Animals were killed 1 month later following auditory brainstem response examination. Histomorphology of cochlea was detected with hematoxylin–eosin staining, and Dot1l expression was examined with immunohistochemistry and Western blot. Results There was no significant difference in ABR thresholds before and after injection of aldosterone or saline in either group. Endolymphatic hydrops was found in 75% of animals in the treatment group. Dot1l was found in both groups in the stria vascularis, Reissner’s membrane, spiral limbus, organ of Corti and spiral ligament. Dot1l expression in the treatment group was decreased by aldosterone. Conclusions Dot1l in guinea pig cochlea is inhibited by aldosterone with induction of endolymphatic hydrops. Dot1l may be closely related to endolymph regulation by aldosterone and to pathogenesis of Meniere’s disease.https://doi.org/10.1186/s40001-023-00994-yDot1lAldosteroneEndolymphatic hydropsMeniere’s disease
spellingShingle Shixun Zhong
Biyun Zhang
Li Qin
Qianying Wang
Xiaoli Luo
Aldosterone inhibits Dot1l expression in guinea pig cochlea
European Journal of Medical Research
Dot1l
Aldosterone
Endolymphatic hydrops
Meniere’s disease
title Aldosterone inhibits Dot1l expression in guinea pig cochlea
title_full Aldosterone inhibits Dot1l expression in guinea pig cochlea
title_fullStr Aldosterone inhibits Dot1l expression in guinea pig cochlea
title_full_unstemmed Aldosterone inhibits Dot1l expression in guinea pig cochlea
title_short Aldosterone inhibits Dot1l expression in guinea pig cochlea
title_sort aldosterone inhibits dot1l expression in guinea pig cochlea
topic Dot1l
Aldosterone
Endolymphatic hydrops
Meniere’s disease
url https://doi.org/10.1186/s40001-023-00994-y
work_keys_str_mv AT shixunzhong aldosteroneinhibitsdot1lexpressioninguineapigcochlea
AT biyunzhang aldosteroneinhibitsdot1lexpressioninguineapigcochlea
AT liqin aldosteroneinhibitsdot1lexpressioninguineapigcochlea
AT qianyingwang aldosteroneinhibitsdot1lexpressioninguineapigcochlea
AT xiaoliluo aldosteroneinhibitsdot1lexpressioninguineapigcochlea