Hyperglycemic stress induces oxidative damage of enteric glial cells by triggering redoxosomes/p66SHC activation

Objectives Diabetic gastrointestinal dysfunction (DGD) is a serious complication of diabetic mellitus (DM), affecting the enteric nervous system (ENS), particular enteric glial cells (EGCs). This study aimed to elucidate the effects and underlying molecular mechanisms of hyperglycemic stress on EGCs...

Full description

Saved in:
Bibliographic Details
Main Authors: Yanmin Jiang, Lan Xu, Xue Zhu, Xiaowei Zhu, Xiang Xu, Jianbo Li
Format: Article
Language:English
Published: Taylor & Francis Group 2024-12-01
Series:Redox Report
Subjects:
Online Access:https://www.tandfonline.com/doi/10.1080/13510002.2024.2324234
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1846138654133583872
author Yanmin Jiang
Lan Xu
Xue Zhu
Xiaowei Zhu
Xiang Xu
Jianbo Li
author_facet Yanmin Jiang
Lan Xu
Xue Zhu
Xiaowei Zhu
Xiang Xu
Jianbo Li
author_sort Yanmin Jiang
collection DOAJ
description Objectives Diabetic gastrointestinal dysfunction (DGD) is a serious complication of diabetic mellitus (DM), affecting the enteric nervous system (ENS), particular enteric glial cells (EGCs). This study aimed to elucidate the effects and underlying molecular mechanisms of hyperglycemic stress on EGCs in in vitro and in vivo models of DM.Methods In in vitro studies, enteric glial cell line CRL-2690 was exposed to hyperglycemia stress, and cell viability, cell apoptosis and oxidative damage were assessed. In in vivo studies, STZ-induced diabetic mice were constructed, and cell apoptosis and oxidative damage of EGCs in the duodenum of DM mice were assessed.Results The results showed that hyperglycemic stress markedly induced oxidative damage of EGCs in in vitro and in vivo models of DM. This damage was found to be dependent on the activation of redoxosomes, which involved the phosphorylation of SRC and Vav2, the up-regulation of active RAC1-GTP, and the activation of NADPH oxidase (NOX). Moreover, inhibitors of redoxosomes, such as the RAC1 inhibitor NSC23766 and the NOX inhibitor VAS2870, effectively mitigated the hyperglycemic stress-induced oxidative damage of EGCs. Additionally, inhibition of p66SHC, a downstream target of redoxosomes, attenuated oxidative damage of EGCs under hyperglycemic stress.Discussion Our findings suggest that the redoxosomes/p66SHC signaling is involved in the oxidative damage of EGCs during the pathological process of DGD. This signaling cascade may represent a potential therapeutic target for the treatment of DGD.
format Article
id doaj-art-1be2eb2f7cc74881bde772e6d4a26c4d
institution Kabale University
issn 1351-0002
1743-2928
language English
publishDate 2024-12-01
publisher Taylor & Francis Group
record_format Article
series Redox Report
spelling doaj-art-1be2eb2f7cc74881bde772e6d4a26c4d2024-12-07T06:20:31ZengTaylor & Francis GroupRedox Report1351-00021743-29282024-12-0129110.1080/13510002.2024.2324234Hyperglycemic stress induces oxidative damage of enteric glial cells by triggering redoxosomes/p66SHC activationYanmin Jiang0Lan Xu1Xue Zhu2Xiaowei Zhu3Xiang Xu4Jianbo Li5Department of Endocrinology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, People’s Republic of ChinaDepartment of Endocrinology, Wuxi Medical Center, The Affiliated Wuxi People's Hospital of Nanjing Medical University, Wuxi People's Hospital, Nanjing Medical University, Wuxi, People’s Republic of ChinaNational Health Commission (NHC) Key Laboratory of Nuclear Medicine, Jiangsu Key Laboratory of Molecular Nuclear Medicine, Jiangsu Institute of Nuclear Medicine, Wuxi, People’s Republic of ChinaDepartment of Endocrinology, Wuxi Medical Center, The Affiliated Wuxi People's Hospital of Nanjing Medical University, Wuxi People's Hospital, Nanjing Medical University, Wuxi, People’s Republic of ChinaDepartment of Endocrinology, Wuxi Medical Center, The Affiliated Wuxi People's Hospital of Nanjing Medical University, Wuxi People's Hospital, Nanjing Medical University, Wuxi, People’s Republic of ChinaDepartment of Endocrinology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, People’s Republic of ChinaObjectives Diabetic gastrointestinal dysfunction (DGD) is a serious complication of diabetic mellitus (DM), affecting the enteric nervous system (ENS), particular enteric glial cells (EGCs). This study aimed to elucidate the effects and underlying molecular mechanisms of hyperglycemic stress on EGCs in in vitro and in vivo models of DM.Methods In in vitro studies, enteric glial cell line CRL-2690 was exposed to hyperglycemia stress, and cell viability, cell apoptosis and oxidative damage were assessed. In in vivo studies, STZ-induced diabetic mice were constructed, and cell apoptosis and oxidative damage of EGCs in the duodenum of DM mice were assessed.Results The results showed that hyperglycemic stress markedly induced oxidative damage of EGCs in in vitro and in vivo models of DM. This damage was found to be dependent on the activation of redoxosomes, which involved the phosphorylation of SRC and Vav2, the up-regulation of active RAC1-GTP, and the activation of NADPH oxidase (NOX). Moreover, inhibitors of redoxosomes, such as the RAC1 inhibitor NSC23766 and the NOX inhibitor VAS2870, effectively mitigated the hyperglycemic stress-induced oxidative damage of EGCs. Additionally, inhibition of p66SHC, a downstream target of redoxosomes, attenuated oxidative damage of EGCs under hyperglycemic stress.Discussion Our findings suggest that the redoxosomes/p66SHC signaling is involved in the oxidative damage of EGCs during the pathological process of DGD. This signaling cascade may represent a potential therapeutic target for the treatment of DGD.https://www.tandfonline.com/doi/10.1080/13510002.2024.2324234Diabetic gastrointestinal dysfunctionenteric glial cellshyperglycemic stressredoxosomes/p66SHC signaling
spellingShingle Yanmin Jiang
Lan Xu
Xue Zhu
Xiaowei Zhu
Xiang Xu
Jianbo Li
Hyperglycemic stress induces oxidative damage of enteric glial cells by triggering redoxosomes/p66SHC activation
Redox Report
Diabetic gastrointestinal dysfunction
enteric glial cells
hyperglycemic stress
redoxosomes/p66SHC signaling
title Hyperglycemic stress induces oxidative damage of enteric glial cells by triggering redoxosomes/p66SHC activation
title_full Hyperglycemic stress induces oxidative damage of enteric glial cells by triggering redoxosomes/p66SHC activation
title_fullStr Hyperglycemic stress induces oxidative damage of enteric glial cells by triggering redoxosomes/p66SHC activation
title_full_unstemmed Hyperglycemic stress induces oxidative damage of enteric glial cells by triggering redoxosomes/p66SHC activation
title_short Hyperglycemic stress induces oxidative damage of enteric glial cells by triggering redoxosomes/p66SHC activation
title_sort hyperglycemic stress induces oxidative damage of enteric glial cells by triggering redoxosomes p66shc activation
topic Diabetic gastrointestinal dysfunction
enteric glial cells
hyperglycemic stress
redoxosomes/p66SHC signaling
url https://www.tandfonline.com/doi/10.1080/13510002.2024.2324234
work_keys_str_mv AT yanminjiang hyperglycemicstressinducesoxidativedamageofentericglialcellsbytriggeringredoxosomesp66shcactivation
AT lanxu hyperglycemicstressinducesoxidativedamageofentericglialcellsbytriggeringredoxosomesp66shcactivation
AT xuezhu hyperglycemicstressinducesoxidativedamageofentericglialcellsbytriggeringredoxosomesp66shcactivation
AT xiaoweizhu hyperglycemicstressinducesoxidativedamageofentericglialcellsbytriggeringredoxosomesp66shcactivation
AT xiangxu hyperglycemicstressinducesoxidativedamageofentericglialcellsbytriggeringredoxosomesp66shcactivation
AT jianboli hyperglycemicstressinducesoxidativedamageofentericglialcellsbytriggeringredoxosomesp66shcactivation