HNF-1β alleviates podocyte injury in lupus nephritis by maintaining endoplasmic reticulum homeostasis

Objective The current study aims to elucidate the critical function of hepatocyte nuclear factor 1-beta (HNF1-β) in lupus nephritis (LN) by investigating its modulation of the Derlin-1/valosin-containing protein (VCP)/VCP-interacting membrane selenoprotein (VIMP) complex, endoplasmic reticulum (ER)...

Full description

Saved in:
Bibliographic Details
Main Authors: Jie Yu, Bing Guo, Fan Zhang, Miao Liu, Ying Xie, Hui-mei Zou, Yuan-yuan Ruan, Xiao-min An, Pei-lei Chen, Ying-qin Luo, Ming-jun Shi, Li-fen Xu
Format: Article
Language:English
Published: BMJ Publishing Group 2024-12-01
Series:Lupus Science and Medicine
Online Access:https://lupus.bmj.com/content/11/2/e001349.full
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1850260887655415808
author Jie Yu
Bing Guo
Fan Zhang
Miao Liu
Ying Xie
Hui-mei Zou
Yuan-yuan Ruan
Xiao-min An
Pei-lei Chen
Ying-qin Luo
Ming-jun Shi
Li-fen Xu
author_facet Jie Yu
Bing Guo
Fan Zhang
Miao Liu
Ying Xie
Hui-mei Zou
Yuan-yuan Ruan
Xiao-min An
Pei-lei Chen
Ying-qin Luo
Ming-jun Shi
Li-fen Xu
author_sort Jie Yu
collection DOAJ
description Objective The current study aims to elucidate the critical function of hepatocyte nuclear factor 1-beta (HNF1-β) in lupus nephritis (LN) by investigating its modulation of the Derlin-1/valosin-containing protein (VCP)/VCP-interacting membrane selenoprotein (VIMP) complex, endoplasmic reticulum (ER) stress and podocyte apoptosis.Methods In vitro and in vivo models of LN were established using glomerular podocytes treated with LN serum and MRL/lpr mice, respectively. The expression levels of HNF1-β were analysed in kidney tissues from patients with LN and MRL/lpr mice. To assess the effects of HNF1-β inhibition, an adeno-associated virus vector carrying HNF1-β short hairpin was administered to MRL/lpr mice. In vitro, glomerular podocytes were transfected with HNF1-β small interfering RNA (siRNA) or HNF1-β overexpression plasmids to explore their regulatory effects on the Derlin-1/VCP/VIMP complex and podocyte apoptosis. Dual-luciferase reporter assays and chromatin immunoprecipitation (ChIP) assays were performed to investigate the transcriptional activation of Derlin-1 and VCP promoters by HNF1-β.Results A significant decrease in HNF1-β levels was observed in kidney tissues from patients with LN while MRL/lpr mice exhibited an initial compensatory increase followed by a subsequent decrease in renal HNF1-β expression. Overexpression of HNF1-β transcriptionally upregulated Derlin-1 and VCP mitigating LN serum-induced ER stress and podocyte apoptosis. In contrast, HNF1-β inhibition exacerbated renal dysfunction and structural damage in MRL/lpr mice. Interestingly, HNF1-β inhibition transcriptionally repressed ERP44, leading to calcium ions (Ca²+) release-mediated disruption and inactivation of the Derlin-1/VCP/VIMP complex. This finding suggests that HNF1-β not only regulates the expression of key proteins in the Derlin-1/VCP/VIMP complex but also influences their assembly through Ca²+ release regulation.Conclusion This study provides novel insights into the regulatory mechanisms of HNF1-β in LN emphasising its impact on the Derlin-1/VCP/VIMP complex, ER stress and podocyte apoptosis. These findings have the potential to inform the development of new diagnostic tools and therapeutic strategies for LN.
format Article
id doaj-art-8f22fbc92f04417db9a4180832effdfe
institution OA Journals
issn 2053-8790
language English
publishDate 2024-12-01
publisher BMJ Publishing Group
record_format Article
series Lupus Science and Medicine
spelling doaj-art-8f22fbc92f04417db9a4180832effdfe2025-08-20T01:55:32ZengBMJ Publishing GroupLupus Science and Medicine2053-87902024-12-0111210.1136/lupus-2024-001349HNF-1β alleviates podocyte injury in lupus nephritis by maintaining endoplasmic reticulum homeostasisJie Yu0Bing Guo1Fan Zhang2Miao Liu3Ying Xie4Hui-mei Zou5Yuan-yuan Ruan6Xiao-min An7Pei-lei Chen8Ying-qin Luo9Ming-jun Shi10Li-fen Xu11Guizhou Provincial Key Laboratory of Pathogenesis and Drug Research on Common Chronic Diseases, Guizhou Medical University, Guiyang, ChinaDepartment of Pathophysiology, Guizhou Medical University, Guiyang, ChinaDepartment of Pathophysiology, Guizhou Medical University, Guiyang, ChinaDepartment of Urinary Surgery, The Affiliated Hospital of Guizhou Medical University, Guiyang, ChinaDepartment of Pathophysiology, Guizhou Medical University, Guiyang, ChinaDepartment of Pathophysiology, Guizhou Medical University, Guiyang, ChinaDepartment of Pathophysiology, Guizhou Medical University, Guiyang, ChinaDepartment of Pathophysiology, Guizhou Medical University, Guiyang, ChinaDepartment of Pathophysiology, Guizhou Medical University, Guiyang, ChinaDepartment of Pathophysiology, Guizhou Medical University, Guiyang, ChinaDepartment of Pathophysiology, Guizhou Medical University, Guiyang, ChinaDepartment of Pathology, The Affiliated Hospital of Guizhou Medical University, Guiyang, ChinaObjective The current study aims to elucidate the critical function of hepatocyte nuclear factor 1-beta (HNF1-β) in lupus nephritis (LN) by investigating its modulation of the Derlin-1/valosin-containing protein (VCP)/VCP-interacting membrane selenoprotein (VIMP) complex, endoplasmic reticulum (ER) stress and podocyte apoptosis.Methods In vitro and in vivo models of LN were established using glomerular podocytes treated with LN serum and MRL/lpr mice, respectively. The expression levels of HNF1-β were analysed in kidney tissues from patients with LN and MRL/lpr mice. To assess the effects of HNF1-β inhibition, an adeno-associated virus vector carrying HNF1-β short hairpin was administered to MRL/lpr mice. In vitro, glomerular podocytes were transfected with HNF1-β small interfering RNA (siRNA) or HNF1-β overexpression plasmids to explore their regulatory effects on the Derlin-1/VCP/VIMP complex and podocyte apoptosis. Dual-luciferase reporter assays and chromatin immunoprecipitation (ChIP) assays were performed to investigate the transcriptional activation of Derlin-1 and VCP promoters by HNF1-β.Results A significant decrease in HNF1-β levels was observed in kidney tissues from patients with LN while MRL/lpr mice exhibited an initial compensatory increase followed by a subsequent decrease in renal HNF1-β expression. Overexpression of HNF1-β transcriptionally upregulated Derlin-1 and VCP mitigating LN serum-induced ER stress and podocyte apoptosis. In contrast, HNF1-β inhibition exacerbated renal dysfunction and structural damage in MRL/lpr mice. Interestingly, HNF1-β inhibition transcriptionally repressed ERP44, leading to calcium ions (Ca²+) release-mediated disruption and inactivation of the Derlin-1/VCP/VIMP complex. This finding suggests that HNF1-β not only regulates the expression of key proteins in the Derlin-1/VCP/VIMP complex but also influences their assembly through Ca²+ release regulation.Conclusion This study provides novel insights into the regulatory mechanisms of HNF1-β in LN emphasising its impact on the Derlin-1/VCP/VIMP complex, ER stress and podocyte apoptosis. These findings have the potential to inform the development of new diagnostic tools and therapeutic strategies for LN.https://lupus.bmj.com/content/11/2/e001349.full
spellingShingle Jie Yu
Bing Guo
Fan Zhang
Miao Liu
Ying Xie
Hui-mei Zou
Yuan-yuan Ruan
Xiao-min An
Pei-lei Chen
Ying-qin Luo
Ming-jun Shi
Li-fen Xu
HNF-1β alleviates podocyte injury in lupus nephritis by maintaining endoplasmic reticulum homeostasis
Lupus Science and Medicine
title HNF-1β alleviates podocyte injury in lupus nephritis by maintaining endoplasmic reticulum homeostasis
title_full HNF-1β alleviates podocyte injury in lupus nephritis by maintaining endoplasmic reticulum homeostasis
title_fullStr HNF-1β alleviates podocyte injury in lupus nephritis by maintaining endoplasmic reticulum homeostasis
title_full_unstemmed HNF-1β alleviates podocyte injury in lupus nephritis by maintaining endoplasmic reticulum homeostasis
title_short HNF-1β alleviates podocyte injury in lupus nephritis by maintaining endoplasmic reticulum homeostasis
title_sort hnf 1β alleviates podocyte injury in lupus nephritis by maintaining endoplasmic reticulum homeostasis
url https://lupus.bmj.com/content/11/2/e001349.full
work_keys_str_mv AT jieyu hnf1balleviatespodocyteinjuryinlupusnephritisbymaintainingendoplasmicreticulumhomeostasis
AT bingguo hnf1balleviatespodocyteinjuryinlupusnephritisbymaintainingendoplasmicreticulumhomeostasis
AT fanzhang hnf1balleviatespodocyteinjuryinlupusnephritisbymaintainingendoplasmicreticulumhomeostasis
AT miaoliu hnf1balleviatespodocyteinjuryinlupusnephritisbymaintainingendoplasmicreticulumhomeostasis
AT yingxie hnf1balleviatespodocyteinjuryinlupusnephritisbymaintainingendoplasmicreticulumhomeostasis
AT huimeizou hnf1balleviatespodocyteinjuryinlupusnephritisbymaintainingendoplasmicreticulumhomeostasis
AT yuanyuanruan hnf1balleviatespodocyteinjuryinlupusnephritisbymaintainingendoplasmicreticulumhomeostasis
AT xiaominan hnf1balleviatespodocyteinjuryinlupusnephritisbymaintainingendoplasmicreticulumhomeostasis
AT peileichen hnf1balleviatespodocyteinjuryinlupusnephritisbymaintainingendoplasmicreticulumhomeostasis
AT yingqinluo hnf1balleviatespodocyteinjuryinlupusnephritisbymaintainingendoplasmicreticulumhomeostasis
AT mingjunshi hnf1balleviatespodocyteinjuryinlupusnephritisbymaintainingendoplasmicreticulumhomeostasis
AT lifenxu hnf1balleviatespodocyteinjuryinlupusnephritisbymaintainingendoplasmicreticulumhomeostasis