MLKL deficiency protects against low-grade, sterile inflammation in aged mice

MLKL and RIPK3 are the core signaling proteins of the inflammatory cell death pathway, necroptosis, which is a known mediator and modifier of human disease. Necroptosis has been implicated in the progression of disease in almost every physiological system and recent reports suggest a role for necrop...

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Published inCell death and differentiation Vol. 30; no. 4; pp. 1059 - 1071
Main Authors Tovey Crutchfield, Emma C., Garnish, Sarah E., Day, Jessica, Anderton, Holly, Chiou, Shene, Hempel, Anne, Hall, Cathrine, Patel, Komal M., Gangatirkar, Pradnya, Martin, Katherine R., Li Wai Suen, Connie S. N., Garnham, Alexandra L., Kueh, Andrew J., Wicks, Ian P., Silke, John, Nachbur, Ueli, Samson, Andre L., Murphy, James M., Hildebrand, Joanne M.
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 01.04.2023
Nature Publishing Group
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Abstract MLKL and RIPK3 are the core signaling proteins of the inflammatory cell death pathway, necroptosis, which is a known mediator and modifier of human disease. Necroptosis has been implicated in the progression of disease in almost every physiological system and recent reports suggest a role for necroptosis in aging. Here, we present the first comprehensive analysis of age-related histopathological and immunological phenotypes in a cohort of Mlkl –/– and Ripk3 –/– mice on a congenic C57BL/6 J genetic background. We show that genetic deletion of Mlkl in female mice interrupts immune system aging, specifically delaying the age-related reduction of circulating lymphocytes. -Seventeen-month-old Mlkl –/– female mice were also protected against age-related chronic sterile inflammation in connective tissue and skeletal muscle relative to wild-type littermate controls, exhibiting a reduced number of immune cell infiltrates in these sites and fewer regenerating myocytes. These observations implicate MLKL in age-related sterile inflammation, suggesting a possible application for long-term anti-necroptotic therapy in humans.
AbstractList MLKL and RIPK3 are the core signaling proteins of the inflammatory cell death pathway, necroptosis, which is a known mediator and modifier of human disease. Necroptosis has been implicated in the progression of disease in almost every physiological system and recent reports suggest a role for necroptosis in aging. Here, we present the first comprehensive analysis of age-related histopathological and immunological phenotypes in a cohort of Mlkl –/– and Ripk3 –/– mice on a congenic C57BL/6 J genetic background. We show that genetic deletion of Mlkl in female mice interrupts immune system aging, specifically delaying the age-related reduction of circulating lymphocytes. -Seventeen-month-old Mlkl –/– female mice were also protected against age-related chronic sterile inflammation in connective tissue and skeletal muscle relative to wild-type littermate controls, exhibiting a reduced number of immune cell infiltrates in these sites and fewer regenerating myocytes. These observations implicate MLKL in age-related sterile inflammation, suggesting a possible application for long-term anti-necroptotic therapy in humans.
MLKL and RIPK3 are the core signaling proteins of the inflammatory cell death pathway, necroptosis, which is a known mediator and modifier of human disease. Necroptosis has been implicated in the progression of disease in almost every physiological system and recent reports suggest a role for necroptosis in aging. Here, we present the first comprehensive analysis of age-related histopathological and immunological phenotypes in a cohort of Mlkl and Ripk3 mice on a congenic C57BL/6 J genetic background. We show that genetic deletion of Mlkl in female mice interrupts immune system aging, specifically delaying the age-related reduction of circulating lymphocytes. -Seventeen-month-old Mlkl female mice were also protected against age-related chronic sterile inflammation in connective tissue and skeletal muscle relative to wild-type littermate controls, exhibiting a reduced number of immune cell infiltrates in these sites and fewer regenerating myocytes. These observations implicate MLKL in age-related sterile inflammation, suggesting a possible application for long-term anti-necroptotic therapy in humans.
MLKL and RIPK3 are the core signaling proteins of the inflammatory cell death pathway, necroptosis, which is a known mediator and modifier of human disease. Necroptosis has been implicated in the progression of disease in almost every physiological system and recent reports suggest a role for necroptosis in aging. Here, we present the first comprehensive analysis of age-related histopathological and immunological phenotypes in a cohort of Mlkl–/– and Ripk3–/– mice on a congenic C57BL/6 J genetic background. We show that genetic deletion of Mlkl in female mice interrupts immune system aging, specifically delaying the age-related reduction of circulating lymphocytes. -Seventeen-month-old Mlkl–/– female mice were also protected against age-related chronic sterile inflammation in connective tissue and skeletal muscle relative to wild-type littermate controls, exhibiting a reduced number of immune cell infiltrates in these sites and fewer regenerating myocytes. These observations implicate MLKL in age-related sterile inflammation, suggesting a possible application for long-term anti-necroptotic therapy in humans.
Author Hall, Cathrine
Chiou, Shene
Anderton, Holly
Li Wai Suen, Connie S. N.
Patel, Komal M.
Hempel, Anne
Garnish, Sarah E.
Kueh, Andrew J.
Nachbur, Ueli
Hildebrand, Joanne M.
Wicks, Ian P.
Murphy, James M.
Tovey Crutchfield, Emma C.
Gangatirkar, Pradnya
Martin, Katherine R.
Garnham, Alexandra L.
Samson, Andre L.
Day, Jessica
Silke, John
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PublicationTitle Cell death and differentiation
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Snippet MLKL and RIPK3 are the core signaling proteins of the inflammatory cell death pathway, necroptosis, which is a known mediator and modifier of human disease....
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StartPage 1059
SubjectTerms 13/95
14/63
59
631/443/7
631/45/275
64/60
82/80
96
96/106
96/2
Aging
Animals
Apoptosis
Biochemistry
Biomedical and Life Sciences
Cell Biology
Cell Cycle Analysis
Cell Death
Connective tissues
Female
Humans
Immune system
Infant
Inflammation
Inflammation - pathology
Life Sciences
Lymphocytes
Mice
Mice, Inbred C57BL
Myocytes
Necroptosis
Necrosis - metabolism
Phenotypes
Protein Kinases - metabolism
Receptor-Interacting Protein Serine-Threonine Kinases - metabolism
Skeletal muscle
Stem Cells
Transcription Factors - metabolism
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Title MLKL deficiency protects against low-grade, sterile inflammation in aged mice
URI https://link.springer.com/article/10.1038/s41418-023-01121-4
https://www.ncbi.nlm.nih.gov/pubmed/36755069
https://www.proquest.com/docview/2794409230
https://search.proquest.com/docview/2774895772
https://pubmed.ncbi.nlm.nih.gov/PMC10070424
Volume 30
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