TREM1/3 Deficiency Impairs Tissue Repair After Acute Kidney Injury and Mitochondrial Metabolic Flexibility in Tubular Epithelial Cells
Long-term sequelae of acute kidney injury (AKI) are associated with incomplete recovery of renal function and the development of chronic kidney disease (CKD), which can be mediated by aberrant innate immune activation, mitochondrial pathology, and accumulation of senescent tubular epithelial cells (...
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| Veröffentlicht in: | Frontiers in immunology Jg. 10; S. 1469 |
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| Abstract | Long-term sequelae of acute kidney injury (AKI) are associated with incomplete recovery of renal function and the development of chronic kidney disease (CKD), which can be mediated by aberrant innate immune activation, mitochondrial pathology, and accumulation of senescent tubular epithelial cells (TECs). Herein, we show that the innate immune receptor Triggering receptor expressed on myeloid cells-1 (TREM-1) links mitochondrial metabolism to tubular epithelial senescence. TREM-1 is expressed by inflammatory and epithelial cells, both players in renal repair after ischemia/reperfusion (IR)-induced AKI. Hence, we subjected WT and TREM1/3 KO mice to different models of renal IR. TREM1/3 KO mice displayed no major differences during the acute phase of injury, but increased mortality was observed in the recovery phase. This detrimental effect was associated with maladaptive repair, characterized by persistent tubular damage, inflammation, fibrosis, and TEC senescence.
, we observed an altered mitochondrial homeostasis and cellular metabolism in TREM1/3 KO primary TECs. This was associated with G2/M arrest and increased ROS accumulation. Further exposure of cells to ROS-generating triggers drove the cells into a stress-induced senescent state, resulting in decreased wound healing capacity. Treatment with a mitochondria anti-oxidant partly prevented the senescent phenotype, suggesting a role for mitochondria herein. In summary, we have unraveled a novel (metabolic) mechanism by which TREM1/3 deficiency drives senescence in TECs. This involves redox imbalance, mitochondrial dysfunction and a decline in cellular metabolic activities. These finding suggest a novel role for TREM-1 in maintaining tubular homeostasis through regulation of mitochondrial metabolic flexibility. |
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| AbstractList | Long-term sequelae of acute kidney injury (AKI) are associated with incomplete recovery of renal function and the development of chronic kidney disease (CKD), which can be mediated by aberrant innate immune activation, mitochondrial pathology, and accumulation of senescent tubular epithelial cells (TECs). Herein, we show that the innate immune receptor Triggering receptor expressed on myeloid cells-1 (TREM-1) links mitochondrial metabolism to tubular epithelial senescence. TREM-1 is expressed by inflammatory and epithelial cells, both players in renal repair after ischemia/reperfusion (IR)-induced AKI. Hence, we subjected WT and TREM1/3 KO mice to different models of renal IR. TREM1/3 KO mice displayed no major differences during the acute phase of injury, but increased mortality was observed in the recovery phase. This detrimental effect was associated with maladaptive repair, characterized by persistent tubular damage, inflammation, fibrosis, and TEC senescence. In vitro, we observed an altered mitochondrial homeostasis and cellular metabolism in TREM1/3 KO primary TECs. This was associated with G2/M arrest and increased ROS accumulation. Further exposure of cells to ROS-generating triggers drove the cells into a stress-induced senescent state, resulting in decreased wound healing capacity. Treatment with a mitochondria anti-oxidant partly prevented the senescent phenotype, suggesting a role for mitochondria herein. In summary, we have unraveled a novel (metabolic) mechanism by which TREM1/3 deficiency drives senescence in TECs. This involves redox imbalance, mitochondrial dysfunction and a decline in cellular metabolic activities. These finding suggest a novel role for TREM-1 in maintaining tubular homeostasis through regulation of mitochondrial metabolic flexibility. Long-term sequelae of acute kidney injury (AKI) are associated with incomplete recovery of renal function and the development of chronic kidney disease (CKD), which can be mediated by aberrant innate immune activation, mitochondrial pathology, and accumulation of senescent tubular epithelial cells (TECs). Herein, we show that the innate immune receptor Triggering receptor expressed on myeloid cells-1 (TREM-1) links mitochondrial metabolism to tubular epithelial senescence. TREM-1 is expressed by inflammatory and epithelial cells, both players in renal repair after ischemia/reperfusion (IR)-induced AKI. Hence, we subjected WT and TREM1/3 KO mice to different models of renal IR. TREM1/3 KO mice displayed no major differences during the acute phase of injury, but increased mortality was observed in the recovery phase. This detrimental effect was associated with maladaptive repair, characterized by persistent tubular damage, inflammation, fibrosis, and TEC senescence. In vitro, we observed an altered mitochondrial homeostasis and cellular metabolism in TREM1/3 KO primary TECs. This was associated with G2/M arrest and increased ROS accumulation. Further exposure of cells to ROS-generating triggers drove the cells into a stress-induced senescent state, resulting in decreased wound healing capacity. Treatment with a mitochondria anti-oxidant partly prevented the senescent phenotype, suggesting a role for mitochondria herein. In summary, we have unraveled a novel (metabolic) mechanism by which TREM1/3 deficiency drives senescence in TECs. This involves redox imbalance, mitochondrial dysfunction and a decline in cellular metabolic activities. These finding suggest a novel role for TREM-1 in maintaining tubular homeostasis through regulation of mitochondrial metabolic flexibility.Long-term sequelae of acute kidney injury (AKI) are associated with incomplete recovery of renal function and the development of chronic kidney disease (CKD), which can be mediated by aberrant innate immune activation, mitochondrial pathology, and accumulation of senescent tubular epithelial cells (TECs). Herein, we show that the innate immune receptor Triggering receptor expressed on myeloid cells-1 (TREM-1) links mitochondrial metabolism to tubular epithelial senescence. TREM-1 is expressed by inflammatory and epithelial cells, both players in renal repair after ischemia/reperfusion (IR)-induced AKI. Hence, we subjected WT and TREM1/3 KO mice to different models of renal IR. TREM1/3 KO mice displayed no major differences during the acute phase of injury, but increased mortality was observed in the recovery phase. This detrimental effect was associated with maladaptive repair, characterized by persistent tubular damage, inflammation, fibrosis, and TEC senescence. In vitro, we observed an altered mitochondrial homeostasis and cellular metabolism in TREM1/3 KO primary TECs. This was associated with G2/M arrest and increased ROS accumulation. Further exposure of cells to ROS-generating triggers drove the cells into a stress-induced senescent state, resulting in decreased wound healing capacity. Treatment with a mitochondria anti-oxidant partly prevented the senescent phenotype, suggesting a role for mitochondria herein. In summary, we have unraveled a novel (metabolic) mechanism by which TREM1/3 deficiency drives senescence in TECs. This involves redox imbalance, mitochondrial dysfunction and a decline in cellular metabolic activities. These finding suggest a novel role for TREM-1 in maintaining tubular homeostasis through regulation of mitochondrial metabolic flexibility. Long-term sequelae of acute kidney injury (AKI) are associated with incomplete recovery of renal function and the development of chronic kidney disease (CKD), which can be mediated by aberrant innate immune activation, mitochondrial pathology, and accumulation of senescent tubular epithelial cells (TECs). Herein, we show that the innate immune receptor Triggering receptor expressed on myeloid cells-1 (TREM-1) links mitochondrial metabolism to tubular epithelial senescence. TREM-1 is expressed by inflammatory and epithelial cells, both players in renal repair after ischemia/reperfusion (IR)-induced AKI. Hence, we subjected WT and TREM1/3 KO mice to different models of renal IR. TREM1/3 KO mice displayed no major differences during the acute phase of injury, but increased mortality was observed in the recovery phase. This detrimental effect was associated with maladaptive repair, characterized by persistent tubular damage, inflammation, fibrosis, and TEC senescence. , we observed an altered mitochondrial homeostasis and cellular metabolism in TREM1/3 KO primary TECs. This was associated with G2/M arrest and increased ROS accumulation. Further exposure of cells to ROS-generating triggers drove the cells into a stress-induced senescent state, resulting in decreased wound healing capacity. Treatment with a mitochondria anti-oxidant partly prevented the senescent phenotype, suggesting a role for mitochondria herein. In summary, we have unraveled a novel (metabolic) mechanism by which TREM1/3 deficiency drives senescence in TECs. This involves redox imbalance, mitochondrial dysfunction and a decline in cellular metabolic activities. These finding suggest a novel role for TREM-1 in maintaining tubular homeostasis through regulation of mitochondrial metabolic flexibility. |
| Author | Tammaro, Alessandra Rampanelli, Elena Colonna, Marco Claessen, Nike Butter, Loes M. Dessing, Mark C. Borrelli, Cristiana Soriani, Alessandra Florquin, Sandrine Scantlebery, Angelique M. L. Leemans, Jaklien C. |
| AuthorAffiliation | 1 Amsterdam UMC, University of Amsterdam , Amsterdam , Netherlands 3 Center for Life Nano Science, Istituto Italiano di Tecnologia , Rome , Italy 2 Laboratory Affiliated With Istituto Pasteur Italia - Fondazione Cenci Bolognetti, Department of Molecular Medicine, Sapienza University of Rome , Rome , Italy 4 Department of Pathology and Immunology, Washington University School of Medicine , St. Louis, MI , United States |
| AuthorAffiliation_xml | – name: 4 Department of Pathology and Immunology, Washington University School of Medicine , St. Louis, MI , United States – name: 2 Laboratory Affiliated With Istituto Pasteur Italia - Fondazione Cenci Bolognetti, Department of Molecular Medicine, Sapienza University of Rome , Rome , Italy – name: 3 Center for Life Nano Science, Istituto Italiano di Tecnologia , Rome , Italy – name: 1 Amsterdam UMC, University of Amsterdam , Amsterdam , Netherlands |
| Author_xml | – sequence: 1 givenname: Alessandra surname: Tammaro fullname: Tammaro, Alessandra – sequence: 2 givenname: Angelique M. L. surname: Scantlebery fullname: Scantlebery, Angelique M. L. – sequence: 3 givenname: Elena surname: Rampanelli fullname: Rampanelli, Elena – sequence: 4 givenname: Cristiana surname: Borrelli fullname: Borrelli, Cristiana – sequence: 5 givenname: Nike surname: Claessen fullname: Claessen, Nike – sequence: 6 givenname: Loes M. surname: Butter fullname: Butter, Loes M. – sequence: 7 givenname: Alessandra surname: Soriani fullname: Soriani, Alessandra – sequence: 8 givenname: Marco surname: Colonna fullname: Colonna, Marco – sequence: 9 givenname: Jaklien C. surname: Leemans fullname: Leemans, Jaklien C. – sequence: 10 givenname: Mark C. surname: Dessing fullname: Dessing, Mark C. – sequence: 11 givenname: Sandrine surname: Florquin fullname: Florquin, Sandrine |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/31354698$$D View this record in MEDLINE/PubMed |
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| CitedBy_id | crossref_primary_10_1016_j_placenta_2021_09_016 crossref_primary_10_1093_burnst_tkae044 crossref_primary_10_1016_j_semnephrol_2019_10_007 crossref_primary_10_3389_fmed_2022_954574 crossref_primary_10_1038_s41577_023_00837_1 crossref_primary_10_2147_DDDT_S473426 crossref_primary_10_1172_JCI167951 crossref_primary_10_1186_s12967_023_04499_4 crossref_primary_10_1002_path_6302 crossref_primary_10_3389_fimmu_2020_01346 crossref_primary_10_3389_fimmu_2022_907387 crossref_primary_10_1038_s41420_022_01205_z crossref_primary_10_1016_j_surg_2022_02_003 crossref_primary_10_1016_j_phrs_2022_106488 crossref_primary_10_1097_CM9_0000000000003197 crossref_primary_10_1186_s12950_021_00278_4 crossref_primary_10_3390_ijms222011253 crossref_primary_10_1007_s10495_023_01847_z crossref_primary_10_3389_fphar_2024_1424968 crossref_primary_10_3389_fphys_2022_954815 |
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| Copyright | Copyright © 2019 Tammaro, Scantlebery, Rampanelli, Borrelli, Claessen, Butter, Soriani, Colonna, Leemans, Dessing and Florquin. 2019 Tammaro, Scantlebery, Rampanelli, Borrelli, Claessen, Butter, Soriani, Colonna, Leemans, Dessing and Florquin |
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| Keywords | tubular cell senescence maladaptive repair renal repair epithelial innate immunity ischemia/reperfusion injury mitochondrial metabolism |
| Language | English |
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| Title | TREM1/3 Deficiency Impairs Tissue Repair After Acute Kidney Injury and Mitochondrial Metabolic Flexibility in Tubular Epithelial Cells |
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