scholarly journals Early Phase Mast Cell Activation Determines the Chronic Outcome of Renal Ischemia–Reperfusion Injury

2017 ◽  
Vol 198 (6) ◽  
pp. 2374-2382 ◽  
Author(s):  
Luca Danelli ◽  
Lydia Celia Madjene ◽  
Iris Madera-Salcedo ◽  
Gregory Gautier ◽  
Emeline Pacreau ◽  
...  
Keyword(s):  
Mast Cell ◽  
Reperfusion Injury ◽  
Early Phase ◽  
Cell Activation ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Mast Cell Activation ◽  
Renal Ischemia Reperfusion Injury

scholarly journals NKT Cell Activation Mediates Neutrophil IFN-γ Production and Renal Ischemia-Reperfusion Injury

2007 ◽  
Vol 178 (9) ◽  
pp. 5899-5911 ◽  
Author(s):  
Li Li ◽  
Liping Huang ◽  
Sun-sang J. Sung ◽  
Peter I. Lobo ◽  
Michael G. Brown ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Cell Activation ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Nkt Cell ◽  
Renal Ischemia Reperfusion Injury ◽  
Ifn Γ

scholarly journals TSC1 Affects the Process of Renal Ischemia-Reperfusion Injury by Controlling Macrophage Polarization

2021 ◽  
Vol 12 ◽  
Author(s):  
Xiao Hu ◽  
Yanan Xu ◽  
Zhaoqi Zhang ◽  
Zuofu Tang ◽  
Jinhua Zhang ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Early Phase ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Macrophage Polarization ◽  
Renal Ischemia ◽  
Negative Regulator ◽  
Activated Macrophages ◽  
Renal Ischemia Reperfusion Injury ◽  
Repair Phase

Renal ischemia-reperfusion injury (IRI) contributes to acute kidney injury (AKI), increases morbidity and mortality, and is a significant risk factor for chronic kidney disease (CKD). Macrophage infiltration is a common feature after renal IRI, and infiltrating macrophages can be polarized into the following two distinct types: M1 macrophages, i.e., classically activated macrophages, which can not only inhibit infection but also accelerate renal injury, and M2 macrophages, i.e., alternatively activated macrophages, which have a repair phenotype that can promote wound healing and subsequent fibrosis. The role of TSC1, which is a negative regulator of mTOR signaling that regulates macrophage polarization in inflammation-linked diseases, has been well documented, but whether TSC1 contributes to macrophage polarization in the process of IRI is still unknown. Here, by using a mouse model of renal ischemia-reperfusion, we found that myeloid cell-specific TSC1 knockout mice (termed Lyz-TSC1 cKO mice) had higher serum creatinine levels, more severe histological damage, and greater proinflammatory cytokine production than wild-type (WT) mice during the early phase after renal ischemia-reperfusion. Furthermore, the Lyz-TSC1 cKO mice showed attenuated renal fibrosis during the repair phase of IRI with decreased levels of M2 markers on macrophages in the operated kidneys, which was further confirmed in a cell model of hypoxia-reoxygenation (H/R) in vitro. Mechanistically, by using RNA sequencing of sorted renal macrophages, we found that the expression of most M1-related genes was upregulated in the Lyz-TSC1 cKO group (Supplemental Table 1) during the early phase. However, C/EBPβ and CD206 expression was decreased during the repair phase compared to in the WT group. Overall, our findings demonstrate that the expression of TSC1 in macrophages contributes to the whole process of IRI but serves as an inflammation suppressor during the early phase and a fibrosis promoter during the repair phase.

1843: Role of Cxcr2 in Renal Ischemia/Reperfusion Injury

2004 ◽  
Vol 171 (4S) ◽  
pp. 487-487
Author(s):  
Motoo Araki ◽  
Masayoshi Miura ◽  
Hiromi Kumon ◽  
John Belperio ◽  
Robert Strieter ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Renal Ischemia Reperfusion Injury
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