Apoptosis-associated speck-like protein containing a CARD-mediated release of matrix metalloproteinase 10 stimulates a change in microglia phenotype
Inflammation contributes to amyloid-β and tau pathology in Alzheimer’s disease (AD). Microglia facilitate an altered immune response that includes microgliosis, upregulation of inflammasome proteins, and elevation of matrix-metalloproteinases (MMPs). Studies of cerebrospinal fluid (CSF) and blood in...
Ausführliche Beschreibung
Autor*in: |
Kathryn E. Sánchez [verfasserIn] Kiran Bhaskar [verfasserIn] Gary A. Rosenberg [verfasserIn] |
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Format: |
E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2022 |
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Schlagwörter: |
apoptosis-associated speck like protein containing a CARD (ASC) |
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Übergeordnetes Werk: |
In: Frontiers in Molecular Neuroscience - Frontiers Media S.A., 2008, 15(2022) |
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Übergeordnetes Werk: |
volume:15 ; year:2022 |
Links: |
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DOI / URN: |
10.3389/fnmol.2022.976108 |
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Katalog-ID: |
DOAJ084433612 |
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10.3389/fnmol.2022.976108 doi (DE-627)DOAJ084433612 (DE-599)DOAJ46de3c30db5347a4b84c8cd043e8ba03 DE-627 ger DE-627 rakwb eng RC321-571 Kathryn E. Sánchez verfasserin aut Apoptosis-associated speck-like protein containing a CARD-mediated release of matrix metalloproteinase 10 stimulates a change in microglia phenotype 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Inflammation contributes to amyloid-β and tau pathology in Alzheimer’s disease (AD). Microglia facilitate an altered immune response that includes microgliosis, upregulation of inflammasome proteins, and elevation of matrix-metalloproteinases (MMPs). Studies of cerebrospinal fluid (CSF) and blood in dementia patients show upregulation of two potential biomarkers of inflammation at the cellular level, MMP10 and apoptosis-associated speck-like protein containing a CARD (ASC). However, little is known about their relationship in the context of brain inflammation. Therefore, we stimulated microglia cultures with purified insoluble ASC speck aggregates and MMP10 to elucidate their role. We found that ASC specks altered microglia shape and stimulated the release of MMP3 and MMP10. Furthermore, MMP10 stimulated microglia released additional MMP10 along with the inflammatory cytokines, tumor-necrosis factor-α (TNFα), Interleukin 6 (IL-6), and CXCL1 CXC motif chemokine ligand 1 (CXCL1). A broad-spectrum MMP inhibitor, GM6001, prevented TNFα release. With these results, we conclude that MMP10 and ASC specks act on microglial cells to propagate inflammation. inflammasome apoptosis-associated speck like protein containing a CARD (ASC) matrix-metalloproteinase 10 (MMP10) microglia cytokine Neurosciences. Biological psychiatry. Neuropsychiatry Kiran Bhaskar verfasserin aut Kiran Bhaskar verfasserin aut Gary A. Rosenberg verfasserin aut Gary A. Rosenberg verfasserin aut In Frontiers in Molecular Neuroscience Frontiers Media S.A., 2008 15(2022) (DE-627)579826449 (DE-600)2452967-9 16625099 nnns volume:15 year:2022 https://doi.org/10.3389/fnmol.2022.976108 kostenfrei https://doaj.org/article/46de3c30db5347a4b84c8cd043e8ba03 kostenfrei https://www.frontiersin.org/articles/10.3389/fnmol.2022.976108/full kostenfrei https://doaj.org/toc/1662-5099 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 15 2022 |
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10.3389/fnmol.2022.976108 doi (DE-627)DOAJ084433612 (DE-599)DOAJ46de3c30db5347a4b84c8cd043e8ba03 DE-627 ger DE-627 rakwb eng RC321-571 Kathryn E. Sánchez verfasserin aut Apoptosis-associated speck-like protein containing a CARD-mediated release of matrix metalloproteinase 10 stimulates a change in microglia phenotype 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Inflammation contributes to amyloid-β and tau pathology in Alzheimer’s disease (AD). Microglia facilitate an altered immune response that includes microgliosis, upregulation of inflammasome proteins, and elevation of matrix-metalloproteinases (MMPs). Studies of cerebrospinal fluid (CSF) and blood in dementia patients show upregulation of two potential biomarkers of inflammation at the cellular level, MMP10 and apoptosis-associated speck-like protein containing a CARD (ASC). However, little is known about their relationship in the context of brain inflammation. Therefore, we stimulated microglia cultures with purified insoluble ASC speck aggregates and MMP10 to elucidate their role. We found that ASC specks altered microglia shape and stimulated the release of MMP3 and MMP10. Furthermore, MMP10 stimulated microglia released additional MMP10 along with the inflammatory cytokines, tumor-necrosis factor-α (TNFα), Interleukin 6 (IL-6), and CXCL1 CXC motif chemokine ligand 1 (CXCL1). A broad-spectrum MMP inhibitor, GM6001, prevented TNFα release. With these results, we conclude that MMP10 and ASC specks act on microglial cells to propagate inflammation. inflammasome apoptosis-associated speck like protein containing a CARD (ASC) matrix-metalloproteinase 10 (MMP10) microglia cytokine Neurosciences. Biological psychiatry. Neuropsychiatry Kiran Bhaskar verfasserin aut Kiran Bhaskar verfasserin aut Gary A. Rosenberg verfasserin aut Gary A. Rosenberg verfasserin aut In Frontiers in Molecular Neuroscience Frontiers Media S.A., 2008 15(2022) (DE-627)579826449 (DE-600)2452967-9 16625099 nnns volume:15 year:2022 https://doi.org/10.3389/fnmol.2022.976108 kostenfrei https://doaj.org/article/46de3c30db5347a4b84c8cd043e8ba03 kostenfrei https://www.frontiersin.org/articles/10.3389/fnmol.2022.976108/full kostenfrei https://doaj.org/toc/1662-5099 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 15 2022 |
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RC321-571 Apoptosis-associated speck-like protein containing a CARD-mediated release of matrix metalloproteinase 10 stimulates a change in microglia phenotype inflammasome apoptosis-associated speck like protein containing a CARD (ASC) matrix-metalloproteinase 10 (MMP10) microglia cytokine |
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apoptosis-associated speck-like protein containing a card-mediated release of matrix metalloproteinase 10 stimulates a change in microglia phenotype |
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Apoptosis-associated speck-like protein containing a CARD-mediated release of matrix metalloproteinase 10 stimulates a change in microglia phenotype |
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Inflammation contributes to amyloid-β and tau pathology in Alzheimer’s disease (AD). Microglia facilitate an altered immune response that includes microgliosis, upregulation of inflammasome proteins, and elevation of matrix-metalloproteinases (MMPs). Studies of cerebrospinal fluid (CSF) and blood in dementia patients show upregulation of two potential biomarkers of inflammation at the cellular level, MMP10 and apoptosis-associated speck-like protein containing a CARD (ASC). However, little is known about their relationship in the context of brain inflammation. Therefore, we stimulated microglia cultures with purified insoluble ASC speck aggregates and MMP10 to elucidate their role. We found that ASC specks altered microglia shape and stimulated the release of MMP3 and MMP10. Furthermore, MMP10 stimulated microglia released additional MMP10 along with the inflammatory cytokines, tumor-necrosis factor-α (TNFα), Interleukin 6 (IL-6), and CXCL1 CXC motif chemokine ligand 1 (CXCL1). A broad-spectrum MMP inhibitor, GM6001, prevented TNFα release. With these results, we conclude that MMP10 and ASC specks act on microglial cells to propagate inflammation. |
abstractGer |
Inflammation contributes to amyloid-β and tau pathology in Alzheimer’s disease (AD). Microglia facilitate an altered immune response that includes microgliosis, upregulation of inflammasome proteins, and elevation of matrix-metalloproteinases (MMPs). Studies of cerebrospinal fluid (CSF) and blood in dementia patients show upregulation of two potential biomarkers of inflammation at the cellular level, MMP10 and apoptosis-associated speck-like protein containing a CARD (ASC). However, little is known about their relationship in the context of brain inflammation. Therefore, we stimulated microglia cultures with purified insoluble ASC speck aggregates and MMP10 to elucidate their role. We found that ASC specks altered microglia shape and stimulated the release of MMP3 and MMP10. Furthermore, MMP10 stimulated microglia released additional MMP10 along with the inflammatory cytokines, tumor-necrosis factor-α (TNFα), Interleukin 6 (IL-6), and CXCL1 CXC motif chemokine ligand 1 (CXCL1). A broad-spectrum MMP inhibitor, GM6001, prevented TNFα release. With these results, we conclude that MMP10 and ASC specks act on microglial cells to propagate inflammation. |
abstract_unstemmed |
Inflammation contributes to amyloid-β and tau pathology in Alzheimer’s disease (AD). Microglia facilitate an altered immune response that includes microgliosis, upregulation of inflammasome proteins, and elevation of matrix-metalloproteinases (MMPs). Studies of cerebrospinal fluid (CSF) and blood in dementia patients show upregulation of two potential biomarkers of inflammation at the cellular level, MMP10 and apoptosis-associated speck-like protein containing a CARD (ASC). However, little is known about their relationship in the context of brain inflammation. Therefore, we stimulated microglia cultures with purified insoluble ASC speck aggregates and MMP10 to elucidate their role. We found that ASC specks altered microglia shape and stimulated the release of MMP3 and MMP10. Furthermore, MMP10 stimulated microglia released additional MMP10 along with the inflammatory cytokines, tumor-necrosis factor-α (TNFα), Interleukin 6 (IL-6), and CXCL1 CXC motif chemokine ligand 1 (CXCL1). A broad-spectrum MMP inhibitor, GM6001, prevented TNFα release. With these results, we conclude that MMP10 and ASC specks act on microglial cells to propagate inflammation. |
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Apoptosis-associated speck-like protein containing a CARD-mediated release of matrix metalloproteinase 10 stimulates a change in microglia phenotype |
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