The Mechanism of Delayed Ischemic Preconditioning in Alleviating Acute Ischemia/Reperfusion Renal Injury through Treg Mediated by Immature CD11c <sup>+</sup> Dendritic Cells

Yang, Wenjuan; Peng, Tao; Shi, Chunli; Cui, Fang; Chen, Menghua; Zhang, Ting

doi:10.1159/000527172

ScienceOpen: research and publishing network

For Publishers

For Researchers

Blog
About

Search
Advanced search

views

recommends

Call for Papers: Digital Platforms and Artificial Intelligence in Dementia

Submit here by August 31, 2025

About Dementia and Geriatric Cognitive Disorders: 2.2 Impact Factor I 4.7 CiteScore I 0.809 Scimago Journal & Country Rank (SJR)

Call for Papers: Epidemiology of CKD and its Complications

Submit here by August 31, 2024

About Kidney and Blood Pressure Research: 2.3 Impact Factor I 4.8 CiteScore I 0.674 Scimago Journal & Country Rank (SJR)

Record: found
Abstract: found
Article: found

Is Open Access

The Mechanism of Delayed Ischemic Preconditioning in Alleviating Acute Ischemia/Reperfusion Renal Injury through Treg Mediated by Immature CD11c ⁺ Dendritic Cells

research-article

Author(s): Wenjuan Yang ^a ^, ^b ^, ^c , Tao Peng ^c , Chunli Shi ^c ^, ^d , Fang Cui ^c , Menghua Chen ^a ^, ^c ^, ^* , Ting Zhang ^a ^, ^c ^, ^**

Publication date (Electronic): 14 November 2022

Journal: Kidney Diseases

Publisher: S. Karger AG

Keywords: Ischemia-reperfusion, Ischemic preconditioning, Dendritic cells, Acute kidney injury

Read this article at

ScienceOpenPublisher PMC

There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

Abstract

Introduction

Renal ischemia-reperfusion injury (IRI) is one of the major causes of acute kidney injury, and its mechanism is complex involving multiple factors, while delayed ischemic preconditioning (DIPC) has a protective effect on the above process. In our previous study, we found that DIPC can exert its protection on renal IRI by inhibiting the maturation of dendritic cells (DCs), but the mechanism has not been clarified. This study aimed to investigate the protective mechanism of DIPC on renal IRI in mice through Treg mediated by immature DCs (imDCs).

Methods

The IRI mice model, DIPC treatment, and conditional CD11c<sup>+</sup> DCs (CD11c-DTR) knockout mice were used to perform our study. The maturation and differentiation of DCs and Treg cells in the kidney and spleen were analyzed by flow cytometry. HE staining was used to evaluate the pathology of the kidney tissue. The level of creatinine (Cr), oxidative stress factors (SOD, MDA), and inflammatory factors (TNF-α, IL-10, IL-4) were also measured. Then, imDCs were co-cultured with HK-2 cells, and apoptosis was analyzed with flow cytometry and PI-Hoechst 33,342 fluorescence staining to assess the apoptosis rate of HK-2 cells under hypoxic-reoxygenated (H/R) conditions.

Results

DIPC could decrease renal Cr levels, alleviate pathological renal damage, and reduce oxidative stress and inflammation caused by IRI. Moreover, DIPC could decrease the number of mature DCs (mDCs) and increase Treg lymphocyte infiltration in the kidney tissue, while the reduction of DCs reversed this process. In addition, our in vitro experiment found that in the H/R model, the apoptosis of HK-2 cells decreased which were co-cultured with imDCs.

Conclusion

DIPC can regulate the differentiation of DCs into imDCs, thus affecting the differentiation level and distribution of Treg cells to exert its protective effect on renal IRI.

Related collections

Most cited references 77

Record: found
Abstract: found
Article: not found

Acute kidney injury

Claudio Ronco, Rinaldo Bellomo, John A. Kellum (2019)

Acute kidney injury (AKI) is defined by a rapid increase in serum creatinine, decrease in urine output, or both. AKI occurs in approximately 10-15% of patients admitted to hospital, while its incidence in intensive care has been reported in more than 50% of patients. Kidney dysfunction or damage can occur over a longer period or follow AKI in a continuum with acute and chronic kidney disease. Biomarkers of kidney injury or stress are new tools for risk assessment and could possibly guide therapy. AKI is not a single disease but rather a loose collection of syndromes as diverse as sepsis, cardiorenal syndrome, and urinary tract obstruction. The approach to a patient with AKI depends on the clinical context and can also vary by resource availability. Although the effectiveness of several widely applied treatments is still controversial, evidence for several interventions, especially when used together, has increased over the past decade.

0 comments Cited 706 times – based on 0 reviews      Review now

Record: found
Abstract: found
Article: not found

Acute Kidney Injury from Sepsis: Current Concepts, Epidemiology, Pathophysiology, Prevention and Treatment

Sadudee Peerapornratana, Carlos Manrique-Caballero, Hernando Gómez … (2019)

Sepsis-associated acute kidney injury (S-AKI) is a frequent complication of the critically ill patient and is associated with unacceptable morbidity and mortality. Prevention of S-AKI is difficult because by the time patients seek medical attention, most have already developed acute kidney injury. Thus, early recognition is crucial to provide supportive treatment and limit further insults. Current diagnostic criteria for acute kidney injury has limited early detection; however, novel biomarkers of kidney stress and damage have been recently validated for risk prediction and early diagnosis of acute kidney injury in the setting of sepsis. Recent evidence shows that microvascular dysfunction, inflammation, and metabolic reprogramming are 3 fundamental mechanisms that may play a role in the development of S-AKI. However, more mechanistic studies are needed to better understand the convoluted pathophysiology of S-AKI and to translate these findings into potential treatment strategies and add to the promising pharmacologic approaches being developed and tested in clinical trials.

0 comments Cited 524 times – based on 0 reviews      Review now

Record: found
Abstract: found
Article: not found

Preconditioning with ischemia: a delay of lethal cell injury in ischemic myocardium.

C Murry, R B Jennings, K. Reimer (1986)

Circulation, 74(5), 1124-1136

0 comments Cited 384 times – based on 0 reviews      Review now

All references

Author and article information

Journal

Journal ID (nlm-ta): Kidney Dis (Basel)

Journal ID (iso-abbrev): Kidney Dis (Basel)

Journal ID (publisher-id): KDD

Title: Kidney Diseases

Publisher: S. Karger AG (Allschwilerstrasse 10, P.O. Box · Postfach · Case postale, CH–4009, Basel, Switzerland · Schweiz · Suisse, Phone: +41 61 306 11 11, Fax: +41 61 306 12 34, karger@karger.com )

ISSN (Print): 2296-9381

ISSN (Electronic): 2296-9357

Publication date Collection: December 2022

Publication date (Electronic): 14 November 2022

Publication date PMC-release: 14 November 2022

Volume: 8

Issue: 6

Pages: 487-499

Affiliations

[1] ^aDepartment of Nephrology, General Hospital of Ningxia Medical University, Yinchuan, China

[2] ^bWuxi People's Hospital, Wuxi, China

[3] ^cNingxia Medical University, Yinchuan, China

[4] ^dDepartment of Molecular Biology, Shanghai Centre for Clinical Laboratory, Shanghai, China

Author notes

*Menghua Chen, nxchenmh@ 123456163.com

**Ting Zhang, zhangting29@ 123456139.com

Article

Publisher ID: kdd-0008-0487

DOI: 10.1159/000527172

PMC ID: 9798836

PubMed ID: 36590681

SO-VID: 7cdcd26f-e305-4b4b-a387-9ca42d82c00e

License:

This article is licensed under the Creative Commons Attribution-NonCommercial 4.0 International License (CC BY-NC). Usage and distribution for commercial purposes requires written permission.

History

Date received : 11 March 2022

Date accepted : 18 September 2022

Date: 2022

Page count

Figures: 7, References: 41, Pages: 13

Funding

This work was supported by the National Natural Science Foundation of China and the Natural Science Foundation of Ningxia (Grant No. 81860129) and (Grant No. 2019AAC02004).