17β-Estradiol promotes angiogenesis of stria vascular in cochlea of C57BL/6J mice.


Journal

European journal of pharmacology
ISSN: 1879-0712
Titre abrégé: Eur J Pharmacol
Pays: Netherlands
ID NLM: 1254354

Informations de publication

Date de publication:
15 Dec 2021
Historique:
received: 04 08 2021
revised: 12 11 2021
accepted: 12 11 2021
pubmed: 26 11 2021
medline: 8 3 2022
entrez: 25 11 2021
Statut: ppublish

Résumé

It is widely accepted that the stria vascularis (SV) in cochlea plays a critical role in the generation of endocochlear potential (EP) and the secretion of the endolymph. 17β-estradiol (E2) is the most potent and abundant endogenous estrogen during the premenopausal period, thus, considered as the reference estrogen. This study aimd to investigate the protective effect of E2 by promoting the expression of vascular endothelial growth factor (VEGF) and thus promoting the vascular regeneration of the SV in elderly mice. After being treated with E2 either in vivo or in vitro, the hearing threshold changes of C57BL/6J elder mice continuously reduced, endothelial cell morphology improved, the number of endothelial cells (ECs) tubular nodes increased significantly, the ability of tubular formation enhanced significantly and the expression of VEGF increased. In vitro, cell model in conjunction with in vivo ovariectomized model was established to demonstrate for the first time that E2 promotes angiogenesis by promoting the secretion of VEGF through the phosphatidylinositol 3-kinase (PI3K)/AKT pathway (PI3K/AKT). In conclusion, E2 demonstrated potent angiogenesis properties with significant protection against Age-Related Hearing Loss (ARHL), which provides a new idea for the improvement of ARHL.

Identifiants

pubmed: 34822791
pii: S0014-2999(21)00798-6
doi: 10.1016/j.ejphar.2021.174642
pii:
doi:

Substances chimiques

Angiogenesis Inducing Agents 0
Vascular Endothelial Growth Factor A 0
vascular endothelial growth factor A, mouse 0
Estradiol 4TI98Z838E

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

174642

Informations de copyright

Copyright © 2021 The Authors. Published by Elsevier B.V. All rights reserved.

Auteurs

Zi-Yi Feng (ZY)

Department of Physiology, Medical College of Jiaxing University, Jiaxing, Zhejiang, 314000, China; Department of Physiology, Medical College of Shihezi University, Shihezi, Xinjiang, 832000, China; Maternal and Child Health Care Hospital, Urumqi, Xinjiang, 830000, China.

Tian-Lan Huang (TL)

Department of Physiology, Medical College of Jiaxing University, Jiaxing, Zhejiang, 314000, China; Department of Physiology, Medical College of Shihezi University, Shihezi, Xinjiang, 832000, China.

Xue-Rui Li (XR)

Department of Physiology, Medical College of Shihezi University, Shihezi, Xinjiang, 832000, China.

Long Chen (L)

Department of Physiology, Medical College of Shihezi University, Shihezi, Xinjiang, 832000, China.

Shuang Deng (S)

Department of Physiology, Medical College of Shihezi University, Shihezi, Xinjiang, 832000, China.

Shao-Ran Xu (SR)

Department of Physiology, Medical College of Shihezi University, Shihezi, Xinjiang, 832000, China.

Ke-Tao Ma (KT)

Department of Physiology, Medical College of Shihezi University, Shihezi, Xinjiang, 832000, China.

Li Li (L)

Department of Physiology, Medical College of Jiaxing University, Jiaxing, Zhejiang, 314000, China. Electronic address: lily7588@163.com.

Jun-Qiang Si (JQ)

Department of Physiology, Medical College of Shihezi University, Shihezi, Xinjiang, 832000, China; Department of Neurobiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, 430000, China. Electronic address: sijunqiang@shzu.edu.cn.

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Classifications MeSH