C9orf72-ALS human iPSC microglia are pro-inflammatory and toxic to co-cultured motor neurons via MMP9
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by progressive motor neuron loss, with additional pathophysiological involvement of non-neuronal cells such as microglia. The commonest ALS-associated genetic variant is a hexanucleotide repeat expansion (HRE) mutation...
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Published in | Nature communications Vol. 14; no. 1; p. 5898 |
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Main Authors | , , , , , , , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
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Nature Publishing Group UK
22.09.2023
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Abstract | Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by progressive motor neuron loss, with additional pathophysiological involvement of non-neuronal cells such as microglia. The commonest ALS-associated genetic variant is a hexanucleotide repeat expansion (HRE) mutation in
C9orf72
. Here, we study its consequences for microglial function using human iPSC-derived microglia. By RNA-sequencing, we identify enrichment of pathways associated with immune cell activation and cyto-/chemokines in C9orf72 HRE mutant microglia versus healthy controls, most prominently after LPS priming. Specifically, LPS-primed C9orf72 HRE mutant microglia show consistently increased expression and release of matrix metalloproteinase-9 (MMP9). LPS-primed C9orf72 HRE mutant microglia are toxic to co-cultured healthy motor neurons, which is ameliorated by concomitant application of an MMP9 inhibitor. Finally, we identify release of dipeptidyl peptidase-4 (DPP4) as a marker for MMP9-dependent microglial dysregulation in co-culture. These results demonstrate cellular dysfunction of C9orf72 HRE mutant microglia, and a non-cell-autonomous role in driving C9orf72-ALS pathophysiology in motor neurons through MMP9 signaling.
The role of microglia in amyotrophic lateral sclerosis (ALS) is unclear. Here, the authors show that iPSC microglia from C9orf72-ALS patients are toxic to motor neurons and identify microglial MMP9 as a potential therapeutic target. |
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AbstractList | Abstract
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by progressive motor neuron loss, with additional pathophysiological involvement of non-neuronal cells such as microglia. The commonest ALS-associated genetic variant is a hexanucleotide repeat expansion (HRE) mutation in
C9orf72
. Here, we study its consequences for microglial function using human iPSC-derived microglia. By RNA-sequencing, we identify enrichment of pathways associated with immune cell activation and cyto-/chemokines in C9orf72 HRE mutant microglia versus healthy controls, most prominently after LPS priming. Specifically, LPS-primed C9orf72 HRE mutant microglia show consistently increased expression and release of matrix metalloproteinase-9 (MMP9). LPS-primed C9orf72 HRE mutant microglia are toxic to co-cultured healthy motor neurons, which is ameliorated by concomitant application of an MMP9 inhibitor. Finally, we identify release of dipeptidyl peptidase-4 (DPP4) as a marker for MMP9-dependent microglial dysregulation in co-culture. These results demonstrate cellular dysfunction of C9orf72 HRE mutant microglia, and a non-cell-autonomous role in driving C9orf72-ALS pathophysiology in motor neurons through MMP9 signaling. Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by progressive motor neuron loss, with additional pathophysiological involvement of non-neuronal cells such as microglia. The commonest ALS-associated genetic variant is a hexanucleotide repeat expansion (HRE) mutation in C9orf72. Here, we study its consequences for microglial function using human iPSC-derived microglia. By RNA-sequencing, we identify enrichment of pathways associated with immune cell activation and cyto-/chemokines in C9orf72 HRE mutant microglia versus healthy controls, most prominently after LPS priming. Specifically, LPS-primed C9orf72 HRE mutant microglia show consistently increased expression and release of matrix metalloproteinase-9 (MMP9). LPS-primed C9orf72 HRE mutant microglia are toxic to co-cultured healthy motor neurons, which is ameliorated by concomitant application of an MMP9 inhibitor. Finally, we identify release of dipeptidyl peptidase-4 (DPP4) as a marker for MMP9-dependent microglial dysregulation in co-culture. These results demonstrate cellular dysfunction of C9orf72 HRE mutant microglia, and a non-cell-autonomous role in driving C9orf72-ALS pathophysiology in motor neurons through MMP9 signaling.The role of microglia in amyotrophic lateral sclerosis (ALS) is unclear. Here, the authors show that iPSC microglia from C9orf72-ALS patients are toxic to motor neurons and identify microglial MMP9 as a potential therapeutic target. Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by progressive motor neuron loss, with additional pathophysiological involvement of non-neuronal cells such as microglia. The commonest ALS-associated genetic variant is a hexanucleotide repeat expansion (HRE) mutation in C9orf72. Here, we study its consequences for microglial function using human iPSC-derived microglia. By RNA-sequencing, we identify enrichment of pathways associated with immune cell activation and cyto-/chemokines in C9orf72 HRE mutant microglia versus healthy controls, most prominently after LPS priming. Specifically, LPS-primed C9orf72 HRE mutant microglia show consistently increased expression and release of matrix metalloproteinase-9 (MMP9). LPS-primed C9orf72 HRE mutant microglia are toxic to co-cultured healthy motor neurons, which is ameliorated by concomitant application of an MMP9 inhibitor. Finally, we identify release of dipeptidyl peptidase-4 (DPP4) as a marker for MMP9-dependent microglial dysregulation in co-culture. These results demonstrate cellular dysfunction of C9orf72 HRE mutant microglia, and a non-cell-autonomous role in driving C9orf72-ALS pathophysiology in motor neurons through MMP9 signaling. Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by progressive motor neuron loss, with additional pathophysiological involvement of non-neuronal cells such as microglia. The commonest ALS-associated genetic variant is a hexanucleotide repeat expansion (HRE) mutation in C9orf72 . Here, we study its consequences for microglial function using human iPSC-derived microglia. By RNA-sequencing, we identify enrichment of pathways associated with immune cell activation and cyto-/chemokines in C9orf72 HRE mutant microglia versus healthy controls, most prominently after LPS priming. Specifically, LPS-primed C9orf72 HRE mutant microglia show consistently increased expression and release of matrix metalloproteinase-9 (MMP9). LPS-primed C9orf72 HRE mutant microglia are toxic to co-cultured healthy motor neurons, which is ameliorated by concomitant application of an MMP9 inhibitor. Finally, we identify release of dipeptidyl peptidase-4 (DPP4) as a marker for MMP9-dependent microglial dysregulation in co-culture. These results demonstrate cellular dysfunction of C9orf72 HRE mutant microglia, and a non-cell-autonomous role in driving C9orf72-ALS pathophysiology in motor neurons through MMP9 signaling. The role of microglia in amyotrophic lateral sclerosis (ALS) is unclear. Here, the authors show that iPSC microglia from C9orf72-ALS patients are toxic to motor neurons and identify microglial MMP9 as a potential therapeutic target. Abstract Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by progressive motor neuron loss, with additional pathophysiological involvement of non-neuronal cells such as microglia. The commonest ALS-associated genetic variant is a hexanucleotide repeat expansion (HRE) mutation in C9orf72. Here, we study its consequences for microglial function using human iPSC-derived microglia. By RNA-sequencing, we identify enrichment of pathways associated with immune cell activation and cyto-/chemokines in C9orf72 HRE mutant microglia versus healthy controls, most prominently after LPS priming. Specifically, LPS-primed C9orf72 HRE mutant microglia show consistently increased expression and release of matrix metalloproteinase-9 (MMP9). LPS-primed C9orf72 HRE mutant microglia are toxic to co-cultured healthy motor neurons, which is ameliorated by concomitant application of an MMP9 inhibitor. Finally, we identify release of dipeptidyl peptidase-4 (DPP4) as a marker for MMP9-dependent microglial dysregulation in co-culture. These results demonstrate cellular dysfunction of C9orf72 HRE mutant microglia, and a non-cell-autonomous role in driving C9orf72-ALS pathophysiology in motor neurons through MMP9 signaling. |
ArticleNumber | 5898 |
Author | Katsikoudi, Antigoni Xu, Yinyan Gray, Elizabeth Nalluru, Sumedha Isaacs, Adrian M. Scaber, Jakub Cramb, Kaitlyn M. L. Morgan, Georgia R. Carroll, Emily Wade-Martins, Richard Turner, Martin R. Farrimond, Lucy Vahsen, Björn F. Carcolé, Mireia Cowley, Sally A. Dafinca, Ruxandra Talbot, Kevin Amein, Benazir Candalija, Ana |
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References | Serio, Patani (CR3) 2018; 36 Vahsen (CR4) 2021; 17 Banerjee (CR28) 2023; 9 Laflamme (CR29) 2019; 8 Nicolas (CR21) 2018; 97 Kaplan (CR22) 2014; 81 Mori (CR11) 2013; 339 Haenseler (CR16) 2017; 8 Fang (CR36) 2010; 294 Dafinca (CR39) 2020; 14 Ilieva, Polymenidou, Cleveland (CR1) 2009; 187 Vahsen (CR17) 2022; 12 Simone (CR20) 2018; 10 Rohrborn, Eckel, Sell (CR26) 2014; 588 Vafadari, Salamian, Kaczmarek (CR34) 2016; 139 Schindelin (CR45) 2012; 9 Love, Huber, Anders (CR43) 2014; 15 van Wilgenburg, Browne, Vowles, Cowley (CR15) 2013; 8 Talbot, Feneberg, Scaber, Thompson, Turner (CR7) 2018; 265 Beckers, Tharkeshwar, Van Damme (CR31) 2021; 17 Beuche (CR35) 2000; 11 Block, Zecca, Hong (CR6) 2007; 8 Liao, Smyth, Shi (CR42) 2014; 30 DeJesus-Hernandez (CR10) 2011; 72 Brettschneider (CR9) 2012; 123 Dafinca, Barbagallo, Talbot (CR32) 2021; 15 Angelopoulou, Piperi (CR37) 2018; 6 Lall (CR14) 2021; 109 Colonna, Butovsky (CR5) 2017; 35 York, LeDue, Bernier, MacVicar (CR19) 2018; 5 Shi (CR30) 2018; 24 Reinhard, Razak, Ethell (CR33) 2015; 9 O’Rourke (CR12) 2016; 351 Spiller (CR23) 2019; 124 Brettschneider (CR8) 2012; 7 McCauley (CR13) 2020; 585 Spiller (CR38) 2018; 21 Kim, Paggi, Park, Bennett, Salzberg (CR41) 2019; 37 Valverde (CR25) 2021; 297 Karlsson (CR40) 2008; 36 von Bartheld, Bahney, Herculano-Houzel (CR24) 2016; 524 Lorenzini (CR27) 2023; 17 Ababneh (CR18) 2020; 29 Yu, Wang, Han, He (CR44) 2012; 16 Chen, Kankel, Su, Han, Ofengeim (CR2) 2018; 25 R Dafinca (41603_CR39) 2020; 14 ME McCauley (41603_CR13) 2020; 585 Y Liao (41603_CR42) 2014; 30 M DeJesus-Hernandez (41603_CR10) 2011; 72 A Kaplan (41603_CR22) 2014; 81 JG O’Rourke (41603_CR12) 2016; 351 W Haenseler (41603_CR16) 2017; 8 J Schindelin (41603_CR45) 2012; 9 J Brettschneider (41603_CR9) 2012; 123 KJ Spiller (41603_CR38) 2018; 21 A Serio (41603_CR3) 2018; 36 L Fang (41603_CR36) 2010; 294 H Ilieva (41603_CR1) 2009; 187 P Banerjee (41603_CR28) 2023; 9 B Vafadari (41603_CR34) 2016; 139 Y Shi (41603_CR30) 2018; 24 K Mori (41603_CR11) 2013; 339 C Laflamme (41603_CR29) 2019; 8 J Brettschneider (41603_CR8) 2012; 7 J Beckers (41603_CR31) 2021; 17 SM Reinhard (41603_CR33) 2015; 9 MI Love (41603_CR43) 2014; 15 BF Vahsen (41603_CR17) 2022; 12 I Lorenzini (41603_CR27) 2023; 17 NA Ababneh (41603_CR18) 2020; 29 ML Block (41603_CR6) 2007; 8 M Colonna (41603_CR5) 2017; 35 R Simone (41603_CR20) 2018; 10 D Lall (41603_CR14) 2021; 109 KJ Spiller (41603_CR23) 2019; 124 R Dafinca (41603_CR32) 2021; 15 D Kim (41603_CR41) 2019; 37 E Angelopoulou (41603_CR37) 2018; 6 BF Vahsen (41603_CR4) 2021; 17 KR Karlsson (41603_CR40) 2008; 36 G Yu (41603_CR44) 2012; 16 EM York (41603_CR19) 2018; 5 A Valverde (41603_CR25) 2021; 297 B van Wilgenburg (41603_CR15) 2013; 8 K Talbot (41603_CR7) 2018; 265 A Nicolas (41603_CR21) 2018; 97 D Rohrborn (41603_CR26) 2014; 588 W Beuche (41603_CR35) 2000; 11 H Chen (41603_CR2) 2018; 25 CS von Bartheld (41603_CR24) 2016; 524 |
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Snippet | Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by progressive motor neuron loss, with additional pathophysiological... Abstract Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by progressive motor neuron loss, with additional pathophysiological... Abstract Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by progressive motor neuron loss, with additional pathophysiological... |
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SubjectTerms | 13/100 13/106 14/19 38/91 631/378/1689/1285 631/378/2596/1953 631/532/2064/2158 Amyotrophic lateral sclerosis Amyotrophic Lateral Sclerosis - genetics C9orf72 Protein - genetics Cell activation Cell culture Chemokines Coculture Techniques Gelatinase B Gene sequencing Genetic diversity Genetic variance Humanities and Social Sciences Humans Immune system Induced Pluripotent Stem Cells Inflammation Lipopolysaccharides Matrix metalloproteinase Matrix Metalloproteinase 9 - genetics Matrix metalloproteinases Metalloproteinase Microglia Motor Neurons multidisciplinary Mutants Neurodegenerative Diseases Neurons Pathophysiology Priming Regulatory sequences Science Science (multidisciplinary) Therapeutic targets |
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Title | C9orf72-ALS human iPSC microglia are pro-inflammatory and toxic to co-cultured motor neurons via MMP9 |
URI | https://link.springer.com/article/10.1038/s41467-023-41603-0 https://www.ncbi.nlm.nih.gov/pubmed/37736756 https://www.proquest.com/docview/2867177440 https://search.proquest.com/docview/2868122009 https://pubmed.ncbi.nlm.nih.gov/PMC10517114 https://doaj.org/article/3d51552885d24a2f94bd75e36ffa3438 |
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