Hydroxychloroquine attenuates renal ischemia/reperfusion injury by inhibiting cathepsin mediated NLRP3 inflammasome activation

Inflammation is a major contributor to the pathogenesis of ischemic acute kidney injury (AKI), which complicates the post-operative outcomes of large numbers of hospitalized surgical patients. Hydroxychloroquine (HCQ), a well-known anti-malarial drug, is commonly used in clinical practice for its an...

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Vydané v:	Cell death & disease Ročník 9; číslo 3; s. 351 - 14
Hlavní autori:	Tang, Tao-Tao, Lv, Lin-Li, Pan, Ming-Ming, Wen, Yi, Wang, Bin, Li, Zuo-Lin, Wu, Min, Wang, Feng-Mei, Crowley, Steve D, Liu, Bi-Cheng
Médium:	Journal Article
Jazyk:	English
Vydavateľské údaje:	London Nature Publishing Group UK 02.03.2018 Springer Nature B.V
Predmet:	13/21 13/51 13/89 14 14/19 38 38/77 64/60 82/80 Acute Kidney Injury - drug therapy Animals Anti-Inflammatory Agents - metabolism Anti-Inflammatory Agents - therapeutic use Antibodies Biochemistry Biomedical and Life Sciences Cathepsin B - metabolism Cathepsin L Cathepsin L - metabolism Cell activation Cell Biology Cell Culture Cell Line Cell Survival - drug effects Creatinine Creatinine - blood Cytoplasm Disease Models, Animal Hepatitis A Virus Cellular Receptor 1 - blood Humans Hydroxychloroquine Hydroxychloroquine - metabolism Hydroxychloroquine - therapeutic use Hypoxia Immunology Inflammasomes Inflammasomes - metabolism Inflammation Ischemia Kidneys Life Sciences Lysosomes Macrophages Macrophages - drug effects Male Mice Mice, Inbred C57BL Neutrophil Infiltration - drug effects NF-kappa B - metabolism NF-κB protein NLR Family, Pyrin Domain-Containing 3 Protein - metabolism Renal function Reperfusion Reperfusion Injury - drug therapy Rodents Surgery
ISSN:	2041-4889, 2041-4889
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Abstract	Inflammation is a major contributor to the pathogenesis of ischemic acute kidney injury (AKI), which complicates the post-operative outcomes of large numbers of hospitalized surgical patients. Hydroxychloroquine (HCQ), a well-known anti-malarial drug, is commonly used in clinical practice for its anti-inflammatory actions. However, little is known about its role in renal ischemia/reperfusion (I/R) injury. In the current study, mice were subjected to I/R injury and HCQ was administered for seven days by gavage prior to surgery. In parallel, HK-2 human renal proximal tubule cells were prophylactically treated with HCQ and then were exposed to hypoxia/reoxygenation (H/R). The results showed that HCQ significantly attenuated renal dysfunction evidenced by blunted decreases in serum creatinine and kidney injury molecular-1 expression and the improvement of HK-2 cell viability. Additionally, HCQ markedly reduced macrophage and neutrophil infiltration, pro-inflammatory cytokine production, and NLRP3 inflammasome activation. Mechanistic studies showed that HCQ could inhibit the priming of the NLRP3 inflammasome by down-regulating I/R or H/R-induced NF-κB signaling. Moreover, HCQ reduced cathepsin (CTS) B, CTSD and CTSL activity, and their redistribution from lysosomes to cytoplasm. CTSB and CTSL (not CTSD) were implicated in I/R triggered NLRP3 inflammasome activation. Notably, we found that HCQ attenuated renal injury through downregulation of CTSB and CTSL-mediated NLRP3 inflammasome activation. This study provides new insights into the anti-inflammatory effect of HCQ in the treatment of AKI.
AbstractList	Inflammation is a major contributor to the pathogenesis of ischemic acute kidney injury (AKI), which complicates the post-operative outcomes of large numbers of hospitalized surgical patients. Hydroxychloroquine (HCQ), a well-known anti-malarial drug, is commonly used in clinical practice for its anti-inflammatory actions. However, little is known about its role in renal ischemia/reperfusion (I/R) injury. In the current study, mice were subjected to I/R injury and HCQ was administered for seven days by gavage prior to surgery. In parallel, HK-2 human renal proximal tubule cells were prophylactically treated with HCQ and then were exposed to hypoxia/reoxygenation (H/R). The results showed that HCQ significantly attenuated renal dysfunction evidenced by blunted decreases in serum creatinine and kidney injury molecular-1 expression and the improvement of HK-2 cell viability. Additionally, HCQ markedly reduced macrophage and neutrophil infiltration, pro-inflammatory cytokine production, and NLRP3 inflammasome activation. Mechanistic studies showed that HCQ could inhibit the priming of the NLRP3 inflammasome by down-regulating I/R or H/R-induced NF-κB signaling. Moreover, HCQ reduced cathepsin (CTS) B, CTSD and CTSL activity, and their redistribution from lysosomes to cytoplasm. CTSB and CTSL (not CTSD) were implicated in I/R triggered NLRP3 inflammasome activation. Notably, we found that HCQ attenuated renal injury through downregulation of CTSB and CTSL-mediated NLRP3 inflammasome activation. This study provides new insights into the anti-inflammatory effect of HCQ in the treatment of AKI. Inflammation is a major contributor to the pathogenesis of ischemic acute kidney injury (AKI), which complicates the post-operative outcomes of large numbers of hospitalized surgical patients. Hydroxychloroquine (HCQ), a well-known anti-malarial drug, is commonly used in clinical practice for its anti-inflammatory actions. However, little is known about its role in renal ischemia/reperfusion (I/R) injury. In the current study, mice were subjected to I/R injury and HCQ was administered for seven days by gavage prior to surgery. In parallel, HK-2 human renal proximal tubule cells were prophylactically treated with HCQ and then were exposed to hypoxia/reoxygenation (H/R). The results showed that HCQ significantly attenuated renal dysfunction evidenced by blunted decreases in serum creatinine and kidney injury molecular-1 expression and the improvement of HK-2 cell viability. Additionally, HCQ markedly reduced macrophage and neutrophil infiltration, pro-inflammatory cytokine production, and NLRP3 inflammasome activation. Mechanistic studies showed that HCQ could inhibit the priming of the NLRP3 inflammasome by down-regulating I/R or H/R-induced NF-κB signaling. Moreover, HCQ reduced cathepsin (CTS) B, CTSD and CTSL activity, and their redistribution from lysosomes to cytoplasm. CTSB and CTSL (not CTSD) were implicated in I/R triggered NLRP3 inflammasome activation. Notably, we found that HCQ attenuated renal injury through downregulation of CTSB and CTSL-mediated NLRP3 inflammasome activation. This study provides new insights into the anti-inflammatory effect of HCQ in the treatment of AKI.Inflammation is a major contributor to the pathogenesis of ischemic acute kidney injury (AKI), which complicates the post-operative outcomes of large numbers of hospitalized surgical patients. Hydroxychloroquine (HCQ), a well-known anti-malarial drug, is commonly used in clinical practice for its anti-inflammatory actions. However, little is known about its role in renal ischemia/reperfusion (I/R) injury. In the current study, mice were subjected to I/R injury and HCQ was administered for seven days by gavage prior to surgery. In parallel, HK-2 human renal proximal tubule cells were prophylactically treated with HCQ and then were exposed to hypoxia/reoxygenation (H/R). The results showed that HCQ significantly attenuated renal dysfunction evidenced by blunted decreases in serum creatinine and kidney injury molecular-1 expression and the improvement of HK-2 cell viability. Additionally, HCQ markedly reduced macrophage and neutrophil infiltration, pro-inflammatory cytokine production, and NLRP3 inflammasome activation. Mechanistic studies showed that HCQ could inhibit the priming of the NLRP3 inflammasome by down-regulating I/R or H/R-induced NF-κB signaling. Moreover, HCQ reduced cathepsin (CTS) B, CTSD and CTSL activity, and their redistribution from lysosomes to cytoplasm. CTSB and CTSL (not CTSD) were implicated in I/R triggered NLRP3 inflammasome activation. Notably, we found that HCQ attenuated renal injury through downregulation of CTSB and CTSL-mediated NLRP3 inflammasome activation. This study provides new insights into the anti-inflammatory effect of HCQ in the treatment of AKI.
ArticleNumber	351
Author	Wu, Min Li, Zuo-Lin Liu, Bi-Cheng Crowley, Steve D Tang, Tao-Tao Lv, Lin-Li Pan, Ming-Ming Wang, Feng-Mei Wen, Yi Wang, Bin
Author_xml	– sequence: 1 givenname: Tao-Tao surname: Tang fullname: Tang, Tao-Tao organization: Institute of Nephrology, Zhong Da Hospital, Southeast University School of Medicine – sequence: 2 givenname: Lin-Li surname: Lv fullname: Lv, Lin-Li email: lvlinli2000@hotmail.com organization: Institute of Nephrology, Zhong Da Hospital, Southeast University School of Medicine – sequence: 3 givenname: Ming-Ming surname: Pan fullname: Pan, Ming-Ming organization: Institute of Nephrology, Zhong Da Hospital, Southeast University School of Medicine – sequence: 4 givenname: Yi surname: Wen fullname: Wen, Yi organization: Institute of Nephrology, Zhong Da Hospital, Southeast University School of Medicine – sequence: 5 givenname: Bin surname: Wang fullname: Wang, Bin organization: Institute of Nephrology, Zhong Da Hospital, Southeast University School of Medicine – sequence: 6 givenname: Zuo-Lin surname: Li fullname: Li, Zuo-Lin organization: Institute of Nephrology, Zhong Da Hospital, Southeast University School of Medicine – sequence: 7 givenname: Min surname: Wu fullname: Wu, Min organization: Institute of Nephrology, Zhong Da Hospital, Southeast University School of Medicine – sequence: 8 givenname: Feng-Mei surname: Wang fullname: Wang, Feng-Mei organization: Institute of Nephrology, Zhong Da Hospital, Southeast University School of Medicine – sequence: 9 givenname: Steve D surname: Crowley fullname: Crowley, Steve D organization: Division of Nephrology, Department of Medicine, Duke University and Durham VA Medical Centers – sequence: 10 givenname: Bi-Cheng surname: Liu fullname: Liu, Bi-Cheng email: liubc64@163.com organization: Institute of Nephrology, Zhong Da Hospital, Southeast University School of Medicine
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PublicationDate	2018-03-02
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PublicationTitle	Cell death & disease
PublicationTitleAbbrev	Cell Death Dis
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PublicationYear	2018
Publisher	Nature Publishing Group UK Springer Nature B.V
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Snippet	Inflammation is a major contributor to the pathogenesis of ischemic acute kidney injury (AKI), which complicates the post-operative outcomes of large numbers...
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SubjectTerms	13/21 13/51 13/89 14 14/19 38 38/77 64/60 82/80 Acute Kidney Injury - drug therapy Animals Anti-Inflammatory Agents - metabolism Anti-Inflammatory Agents - therapeutic use Antibodies Biochemistry Biomedical and Life Sciences Cathepsin B - metabolism Cathepsin L Cathepsin L - metabolism Cell activation Cell Biology Cell Culture Cell Line Cell Survival - drug effects Creatinine Creatinine - blood Cytoplasm Disease Models, Animal Hepatitis A Virus Cellular Receptor 1 - blood Humans Hydroxychloroquine Hydroxychloroquine - metabolism Hydroxychloroquine - therapeutic use Hypoxia Immunology Inflammasomes Inflammasomes - metabolism Inflammation Ischemia Kidneys Life Sciences Lysosomes Macrophages Macrophages - drug effects Male Mice Mice, Inbred C57BL Neutrophil Infiltration - drug effects NF-kappa B - metabolism NF-κB protein NLR Family, Pyrin Domain-Containing 3 Protein - metabolism Renal function Reperfusion Reperfusion Injury - drug therapy Rodents Surgery
Title	Hydroxychloroquine attenuates renal ischemia/reperfusion injury by inhibiting cathepsin mediated NLRP3 inflammasome activation
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