Pathogenesis of lupus nephritis: RIP3 dependent necroptosis and NLRP3 inflammasome activation
RIP3 activation leads to activation of necroptosis and the NLRP3 inflammasome pathways. The activation of RIP3 in lupus nephritis (LN) has not been investigated. In this study, RIP3 and necroptosis pathway activations were demonstrated in podocytes in renal biopsies from patients with class IV LN an...
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| Published in | Journal of autoimmunity Vol. 103; p. 102286 |
|---|---|
| Main Authors | , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
England
Elsevier Ltd
01.09.2019
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| Abstract | RIP3 activation leads to activation of necroptosis and the NLRP3 inflammasome pathways. The activation of RIP3 in lupus nephritis (LN) has not been investigated. In this study, RIP3 and necroptosis pathway activations were demonstrated in podocytes in renal biopsies from patients with class IV LN and in the diseased kidneys from lupus-prone NZM2328 and MRL/lpr mice. RIP3 activation was accompanied with the activation of MLKL, the effector molecule of the necroptosis pathway, and activation of caspase-1, the effector of the NLRP3 inflammasome pathway. Podocyte activation of RIP3 was detected readily with the development of LN in NZM2328 mice, suggesting this activation may play a significant role in the pathogenesis of LN. GSK872, a RIP3 specific inhibitor, inhibited the development of LN in MRL/lpr mice with down-regulation of RIP3 activation in podocytes, decreased the splenic sizes and weights and anti-dsDNA antibody titers. IgG from pooled sera of diseased NZM2328 mice succumbing to LN induced both the necroptosis pathway and NLRP3 inflammasome activation in a podocyte cell line and this activation was specifically blocked by GSK872. These results indicate that the necroptosis pathway and the RIP3 dependent NLRP3 inflammasome pathway are activated in podocytes during LN. Inhibition of RIP3 kinase may be a novel therapeutic approach to treat LN and systemic lupus erythematosus (SLE).
•Necroptosis and NLRP3 inflammasome pathways are activated in podocytes in LN.•RIP3 regulates both NLRP3 inflammasome and necroptosis activation.•IgG from LN activates RIP3 dependent necroptosis and NLRP3 inflammasome pathways.•Inhibition of RIP3 reduces autoimmunity and alleviates clinical manifestation of LN. |
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| AbstractList | RIP3 activation leads to activation of necroptosis and the NLRP3 inflammasome pathways. The activation of RIP3 in lupus nephritis (LN) has not been investigated. In this study, RIP3 and necroptosis pathway activations were demonstrated in podocytes in renal biopsies from patients with class IV LN and in the diseased kidneys from lupus-prone NZM2328 and MRL/
lpr
mice. RIP3 activation was accompanied with the activation of MLKL, the effector molecule of the necroptosis pathway, and activation of caspase-1, the effector of the NLRP3 inflammasome pathway. Podocyte activation of RIP3 was detected readily with the development of LN in NZM2328 mice, suggesting this activation may play a significant role in the pathogenesis of LN. GSK872, a RIP3 specific inhibitor, inhibited the development of LN in MRL/
lpr
mice with down-regulation of RIP3 activation in podocytes, decreased the splenic sizes and weights and anti-dsDNA antibody titers. IgG from pooled sera of diseased NZM2328 mice succumbing to LN induced both the necroptosis pathway and NLRP3 inflammasome activation in a podocyte cell line and this activation was specifically blocked by GSK872. These results indicate that the necroptosis pathway and the RIP3 dependent NLRP3 inflammasome pathway are activated in podocytes during LN. Inhibition of RIP3 kinase may be a novel therapeutic approach to treat LN and systemic lupus erythematosus (SLE). RIP3 activation leads to activation of necroptosis and the NLRP3 inflammasome pathways. The activation of RIP3 in lupus nephritis (LN) has not been investigated. In this study, RIP3 and necroptosis pathway activations were demonstrated in podocytes in renal biopsies from patients with class IV LN and in the diseased kidneys from lupus-prone NZM2328 and MRL/lpr mice. RIP3 activation was accompanied with the activation of MLKL, the effector molecule of the necroptosis pathway, and activation of caspase-1, the effector of the NLRP3 inflammasome pathway. Podocyte activation of RIP3 was detected readily with the development of LN in NZM2328 mice, suggesting this activation may play a significant role in the pathogenesis of LN. GSK872, a RIP3 specific inhibitor, inhibited the development of LN in MRL/lpr mice with down-regulation of RIP3 activation in podocytes, decreased the splenic sizes and weights and anti-dsDNA antibody titers. IgG from pooled sera of diseased NZM2328 mice succumbing to LN induced both the necroptosis pathway and NLRP3 inflammasome activation in a podocyte cell line and this activation was specifically blocked by GSK872. These results indicate that the necroptosis pathway and the RIP3 dependent NLRP3 inflammasome pathway are activated in podocytes during LN. Inhibition of RIP3 kinase may be a novel therapeutic approach to treat LN and systemic lupus erythematosus (SLE). RIP3 activation leads to activation of necroptosis and the NLRP3 inflammasome pathways. The activation of RIP3 in lupus nephritis (LN) has not been investigated. In this study, RIP3 and necroptosis pathway activations were demonstrated in podocytes in renal biopsies from patients with class IV LN and in the diseased kidneys from lupus-prone NZM2328 and MRL/lpr mice. RIP3 activation was accompanied with the activation of MLKL, the effector molecule of the necroptosis pathway, and activation of caspase-1, the effector of the NLRP3 inflammasome pathway. Podocyte activation of RIP3 was detected readily with the development of LN in NZM2328 mice, suggesting this activation may play a significant role in the pathogenesis of LN. GSK872, a RIP3 specific inhibitor, inhibited the development of LN in MRL/lpr mice with down-regulation of RIP3 activation in podocytes, decreased the splenic sizes and weights and anti-dsDNA antibody titers. IgG from pooled sera of diseased NZM2328 mice succumbing to LN induced both the necroptosis pathway and NLRP3 inflammasome activation in a podocyte cell line and this activation was specifically blocked by GSK872. These results indicate that the necroptosis pathway and the RIP3 dependent NLRP3 inflammasome pathway are activated in podocytes during LN. Inhibition of RIP3 kinase may be a novel therapeutic approach to treat LN and systemic lupus erythematosus (SLE). •Necroptosis and NLRP3 inflammasome pathways are activated in podocytes in LN.•RIP3 regulates both NLRP3 inflammasome and necroptosis activation.•IgG from LN activates RIP3 dependent necroptosis and NLRP3 inflammasome pathways.•Inhibition of RIP3 reduces autoimmunity and alleviates clinical manifestation of LN. RIP3 activation leads to activation of necroptosis and the NLRP3 inflammasome pathways. The activation of RIP3 in lupus nephritis (LN) has not been investigated. In this study, RIP3 and necroptosis pathway activations were demonstrated in podocytes in renal biopsies from patients with class IV LN and in the diseased kidneys from lupus-prone NZM2328 and MRL/lpr mice. RIP3 activation was accompanied with the activation of MLKL, the effector molecule of the necroptosis pathway, and activation of caspase-1, the effector of the NLRP3 inflammasome pathway. Podocyte activation of RIP3 was detected readily with the development of LN in NZM2328 mice, suggesting this activation may play a significant role in the pathogenesis of LN. GSK872, a RIP3 specific inhibitor, inhibited the development of LN in MRL/lpr mice with down-regulation of RIP3 activation in podocytes, decreased the splenic sizes and weights and anti-dsDNA antibody titers. IgG from pooled sera of diseased NZM2328 mice succumbing to LN induced both the necroptosis pathway and NLRP3 inflammasome activation in a podocyte cell line and this activation was specifically blocked by GSK872. These results indicate that the necroptosis pathway and the RIP3 dependent NLRP3 inflammasome pathway are activated in podocytes during LN. Inhibition of RIP3 kinase may be a novel therapeutic approach to treat LN and systemic lupus erythematosus (SLE).RIP3 activation leads to activation of necroptosis and the NLRP3 inflammasome pathways. The activation of RIP3 in lupus nephritis (LN) has not been investigated. In this study, RIP3 and necroptosis pathway activations were demonstrated in podocytes in renal biopsies from patients with class IV LN and in the diseased kidneys from lupus-prone NZM2328 and MRL/lpr mice. RIP3 activation was accompanied with the activation of MLKL, the effector molecule of the necroptosis pathway, and activation of caspase-1, the effector of the NLRP3 inflammasome pathway. Podocyte activation of RIP3 was detected readily with the development of LN in NZM2328 mice, suggesting this activation may play a significant role in the pathogenesis of LN. GSK872, a RIP3 specific inhibitor, inhibited the development of LN in MRL/lpr mice with down-regulation of RIP3 activation in podocytes, decreased the splenic sizes and weights and anti-dsDNA antibody titers. IgG from pooled sera of diseased NZM2328 mice succumbing to LN induced both the necroptosis pathway and NLRP3 inflammasome activation in a podocyte cell line and this activation was specifically blocked by GSK872. These results indicate that the necroptosis pathway and the RIP3 dependent NLRP3 inflammasome pathway are activated in podocytes during LN. Inhibition of RIP3 kinase may be a novel therapeutic approach to treat LN and systemic lupus erythematosus (SLE). |
| ArticleNumber | 102286 |
| Author | Huang, Yuefang Gaskin, Felicia Zhou, Mianjing Fu, Rong Hu, Haoqiang Fu, Shu Man Guo, Chaohuan Wang, Shuang Zhao, Jijun Yang, Niansheng |
| AuthorAffiliation | 1 Department of Rheumatology, First Affiliated Hospital, Sun Yat-sen University, Guangzhou, PR China 6 Division of Rheumatology and Center of Inflammation, Immunology and Regenerative Medicine, Department of Medicine and Department of Microbiology, Immunology and Cancer Biology, University of Virginia, Charlottesville, VA 22908-0133, USA 3 Department of Pediatrics, First Affiliated Hospital, Sun Yat-sen University, Guangzhou, PR China 2 Department of Rheumatology, Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, PR China 5 Department of Psychiatry and Neurobehavioral Sciences, University of Virginia, Charlottesville, VA 22908-0203, USA 4 Department of Nephrology, Dongguan People’s Hospital, Dongguan, PR China |
| AuthorAffiliation_xml | – name: 6 Division of Rheumatology and Center of Inflammation, Immunology and Regenerative Medicine, Department of Medicine and Department of Microbiology, Immunology and Cancer Biology, University of Virginia, Charlottesville, VA 22908-0133, USA – name: 1 Department of Rheumatology, First Affiliated Hospital, Sun Yat-sen University, Guangzhou, PR China – name: 5 Department of Psychiatry and Neurobehavioral Sciences, University of Virginia, Charlottesville, VA 22908-0203, USA – name: 3 Department of Pediatrics, First Affiliated Hospital, Sun Yat-sen University, Guangzhou, PR China – name: 4 Department of Nephrology, Dongguan People’s Hospital, Dongguan, PR China – name: 2 Department of Rheumatology, Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, PR China |
| Author_xml | – sequence: 1 givenname: Chaohuan surname: Guo fullname: Guo, Chaohuan organization: Department of Rheumatology, First Affiliated Hospital, Sun Yat-sen University, Guangzhou, PR China – sequence: 2 givenname: Rong surname: Fu fullname: Fu, Rong organization: Department of Rheumatology, Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, PR China – sequence: 3 givenname: Mianjing surname: Zhou fullname: Zhou, Mianjing organization: Department of Rheumatology, First Affiliated Hospital, Sun Yat-sen University, Guangzhou, PR China – sequence: 4 givenname: Shuang surname: Wang fullname: Wang, Shuang organization: Department of Rheumatology, First Affiliated Hospital, Sun Yat-sen University, Guangzhou, PR China – sequence: 5 givenname: Yuefang surname: Huang fullname: Huang, Yuefang organization: Department of Pediatrics, First Affiliated Hospital, Sun Yat-sen University, Guangzhou, PR China – sequence: 6 givenname: Haoqiang surname: Hu fullname: Hu, Haoqiang organization: Department of Nephrology, Dongguan People's Hospital, Dongguan, PR China – sequence: 7 givenname: Jijun surname: Zhao fullname: Zhao, Jijun organization: Department of Rheumatology, First Affiliated Hospital, Sun Yat-sen University, Guangzhou, PR China – sequence: 8 givenname: Felicia surname: Gaskin fullname: Gaskin, Felicia organization: Department of Psychiatry and Neurobehavioral Sciences, University of Virginia, Charlottesville, VA, 22908-0203, USA – sequence: 9 givenname: Niansheng surname: Yang fullname: Yang, Niansheng email: zsuyns@163.com organization: Department of Rheumatology, First Affiliated Hospital, Sun Yat-sen University, Guangzhou, PR China – sequence: 10 givenname: Shu Man surname: Fu fullname: Fu, Shu Man organization: Division of Rheumatology and Center of Inflammation, Immunology and Regenerative Medicine, Department of Medicine and Department of Microbiology, Immunology and Cancer Biology, University of Virginia, Charlottesville, VA, 22908-0133, USA |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/31133359$$D View this record in MEDLINE/PubMed |
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| Keywords | Podocyte Lupus nephritis RIP3 NLRP3 inflammasome Necroptosis |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 These authors contributed equally to this work. Acquisition of data. C. Guo, R. Fu, M. Zhou, S. Wang, Y. Huang, H. Hu, J. Zhao, N. Yang. Analysis and interpretation of data. C. Guo, R. Fu, M. Zhou, S. Wang, Y. Huang, H. Hu, J. Zhao, F. Gaskin, N. Yang and S.M. Fu. All authors were involved in drafting and revising the article, and all authors approved the final version to be published. Dr. Yang had full access to all of the data in the study and took responsibility for the integrity of the data and the accuracy of the data analysis. Study conception and design. C. Guo, R. Fu, M. Zhou, F Gaskin, N. Yang and S.M. Fu. |
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| Title | Pathogenesis of lupus nephritis: RIP3 dependent necroptosis and NLRP3 inflammasome activation |
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