NLRX1 dampens oxidative stress and apoptosis in tissue injury via control of mitochondrial activity

Mitochondrial dysfunction is the most prominent source of oxidative stress in acute and chronic kidney disease. NLRX1 is a receptor of the innate immune system that is ubiquitously expressed and localized in mitochondria. We investigated whether NLRX1 may act at the interface of metabolism and innat...

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Vydáno v:	The Journal of experimental medicine Ročník 214; číslo 8; s. 2405
Hlavní autoři:	Stokman, Geurt, Kors, Lotte, Bakker, Pieter J, Rampanelli, Elena, Claessen, Nike, Teske, Gwendoline J D, Butter, Loes, van Andel, Harmen, van den Bergh Weerman, Marius A, Larsen, Per W B, Dessing, Mark C, Zuurbier, Coert J, Girardin, Stephen E, Florquin, Sandrine, Leemans, Jaklien C
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	United States 07.08.2017
Témata:	Animals Apoptosis - physiology Disease Models, Animal Humans Ischemia - physiopathology Kidney - blood supply Kidney - metabolism Kidney - physiopathology Male Mice, Inbred C57BL Mitochondria - physiology Mitochondrial Proteins - physiology Oxidative Stress - physiology Reperfusion Injury - physiopathology
ISSN:	1540-9538, 1540-9538
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Abstract	Mitochondrial dysfunction is the most prominent source of oxidative stress in acute and chronic kidney disease. NLRX1 is a receptor of the innate immune system that is ubiquitously expressed and localized in mitochondria. We investigated whether NLRX1 may act at the interface of metabolism and innate immunity in a model of oxidative stress. Using a chimeric mouse model for renal ischemia-reperfusion injury, we found that NLRX1 protects against mortality, mitochondrial damage, and epithelial cell apoptosis in an oxidative stress-dependent fashion. We found that NLRX1 regulates oxidative phosphorylation and cell integrity, whereas loss of NLRX1 results in increased oxygen consumption, oxidative stress, and subsequently apoptosis in epithelial cells during ischemia-reperfusion injury. In line, we found that NLRX1 expression in human kidneys decreased during acute renal ischemic injury and acute cellular rejection. Although first implicated in immune regulation, we propose that NLRX1 function extends to the control of mitochondrial activity and prevention of oxidative stress and apoptosis in tissue injury.
AbstractList	Mitochondrial dysfunction is the most prominent source of oxidative stress in acute and chronic kidney disease. NLRX1 is a receptor of the innate immune system that is ubiquitously expressed and localized in mitochondria. We investigated whether NLRX1 may act at the interface of metabolism and innate immunity in a model of oxidative stress. Using a chimeric mouse model for renal ischemia-reperfusion injury, we found that NLRX1 protects against mortality, mitochondrial damage, and epithelial cell apoptosis in an oxidative stress-dependent fashion. We found that NLRX1 regulates oxidative phosphorylation and cell integrity, whereas loss of NLRX1 results in increased oxygen consumption, oxidative stress, and subsequently apoptosis in epithelial cells during ischemia-reperfusion injury. In line, we found that NLRX1 expression in human kidneys decreased during acute renal ischemic injury and acute cellular rejection. Although first implicated in immune regulation, we propose that NLRX1 function extends to the control of mitochondrial activity and prevention of oxidative stress and apoptosis in tissue injury.Mitochondrial dysfunction is the most prominent source of oxidative stress in acute and chronic kidney disease. NLRX1 is a receptor of the innate immune system that is ubiquitously expressed and localized in mitochondria. We investigated whether NLRX1 may act at the interface of metabolism and innate immunity in a model of oxidative stress. Using a chimeric mouse model for renal ischemia-reperfusion injury, we found that NLRX1 protects against mortality, mitochondrial damage, and epithelial cell apoptosis in an oxidative stress-dependent fashion. We found that NLRX1 regulates oxidative phosphorylation and cell integrity, whereas loss of NLRX1 results in increased oxygen consumption, oxidative stress, and subsequently apoptosis in epithelial cells during ischemia-reperfusion injury. In line, we found that NLRX1 expression in human kidneys decreased during acute renal ischemic injury and acute cellular rejection. Although first implicated in immune regulation, we propose that NLRX1 function extends to the control of mitochondrial activity and prevention of oxidative stress and apoptosis in tissue injury. Mitochondrial dysfunction is the most prominent source of oxidative stress in acute and chronic kidney disease. NLRX1 is a receptor of the innate immune system that is ubiquitously expressed and localized in mitochondria. We investigated whether NLRX1 may act at the interface of metabolism and innate immunity in a model of oxidative stress. Using a chimeric mouse model for renal ischemia-reperfusion injury, we found that NLRX1 protects against mortality, mitochondrial damage, and epithelial cell apoptosis in an oxidative stress-dependent fashion. We found that NLRX1 regulates oxidative phosphorylation and cell integrity, whereas loss of NLRX1 results in increased oxygen consumption, oxidative stress, and subsequently apoptosis in epithelial cells during ischemia-reperfusion injury. In line, we found that NLRX1 expression in human kidneys decreased during acute renal ischemic injury and acute cellular rejection. Although first implicated in immune regulation, we propose that NLRX1 function extends to the control of mitochondrial activity and prevention of oxidative stress and apoptosis in tissue injury.
Author	Kors, Lotte Leemans, Jaklien C Rampanelli, Elena Teske, Gwendoline J D Larsen, Per W B Claessen, Nike Dessing, Mark C van Andel, Harmen Butter, Loes Girardin, Stephen E van den Bergh Weerman, Marius A Stokman, Geurt Bakker, Pieter J Florquin, Sandrine Zuurbier, Coert J
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SubjectTerms	Animals Apoptosis - physiology Disease Models, Animal Humans Ischemia - physiopathology Kidney - blood supply Kidney - metabolism Kidney - physiopathology Male Mice, Inbred C57BL Mitochondria - physiology Mitochondrial Proteins - physiology Oxidative Stress - physiology Reperfusion Injury - physiopathology
Title	NLRX1 dampens oxidative stress and apoptosis in tissue injury via control of mitochondrial activity
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