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000257344 037__ $$aDZNE-2023-00413
000257344 041__ $$aEnglish
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000257344 1001_ $$0P:(DE-2719)9001349$$aBraatz, Charlotte$$b0
000257344 245__ $$aNLRP3-directed antisense oligonucleotides reduce microglial immunoactivities in vitro.
000257344 260__ $$aOxford$$bWiley-Blackwell$$c2024
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000257344 520__ $$aAlzheimer's disease (AD) is associated with the cerebral deposition of Amyloid-β (Aβ) peptide, which leads to NLRP3 inflammasome activation and subsequent release of interleukin-1β (IL-1β) and interleukin-18 (IL-18). NLRP3 reduction has been found to increase microglial clearance, protect from synapse loss, and suppress both the changes to synaptic plasticity and spatial memory dysfunction observed in murine AD models. Here, we test whether NLRP3-directed antisense oligonucleotides (ASOs) can be harnessed as immune modulators in primary murine microglia and human THP-1 cells. NLRP3 mRNA degradation was achieved at 72 h of ASO treatment in primary murine microglia. Consequently, NLRP3-directed ASOs significantly reduced the levels of cleaved caspase-1 and mature IL-1β when microglia were either activated by LPS and nigericin or LPS and Aβ. In human THP-1 cells NLRP3-targeted ASOs also significantly reduced the LPS plus nigericin- or LPS plus Aβ-induced release of mature IL-1β. Together, NLRP3-directed ASOs can suppress NLRP3 inflammasome activity and subsequent release of IL-1β in primary murine microglia and THP-1 cells. ASOs may represent a new and alternative approach to modulate NLRP3 inflammasome activation in neurodegenerative diseases, in addition to attempts to inhibit the complex pharmacologically.
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000257344 650_7 $$2Other$$aAlzheimer's disease
000257344 650_7 $$2Other$$aAβ
000257344 650_7 $$2Other$$aNLRP3 inflammasome
000257344 650_7 $$2Other$$aantisense oligonucleotides
000257344 650_7 $$2Other$$ainnate immunity
000257344 650_7 $$2Other$$amicroglia
000257344 650_7 $$2Other$$aneuroinflammation
000257344 650_2 $$2MeSH$$aMicroglia: metabolism
000257344 650_2 $$2MeSH$$aMicroglia: drug effects
000257344 650_2 $$2MeSH$$aAnimals
000257344 650_2 $$2MeSH$$aNLR Family, Pyrin Domain-Containing 3 Protein: metabolism
000257344 650_2 $$2MeSH$$aHumans
000257344 650_2 $$2MeSH$$aMice
000257344 650_2 $$2MeSH$$aOligonucleotides, Antisense: pharmacology
000257344 650_2 $$2MeSH$$aMice, Inbred C57BL
000257344 650_2 $$2MeSH$$aAmyloid beta-Peptides: metabolism
000257344 650_2 $$2MeSH$$aInterleukin-1beta: metabolism
000257344 650_2 $$2MeSH$$aInflammasomes: metabolism
000257344 650_2 $$2MeSH$$aTHP-1 Cells
000257344 650_2 $$2MeSH$$aCells, Cultured
000257344 7001_ $$0P:(DE-2719)9001384$$aKomes, Max$$b1
000257344 7001_ $$0P:(DE-2719)9002244$$aRavichandran, Kishore$$b2
000257344 7001_ $$0P:(DE-2719)9001602$$aGarcia de Fragas, Matheus$$b3
000257344 7001_ $$0P:(DE-2719)2811029$$aGriep, Angelika$$b4
000257344 7001_ $$0P:(DE-2719)9000454$$aSchwartz, Stephanie$$b5
000257344 7001_ $$0P:(DE-2719)2811671$$aMcManus, Roisin$$b6$$eLast author
000257344 7001_ $$0P:(DE-2719)2000008$$aHeneka, Michael T$$b7$$eLast author
000257344 770__ $$aNeuroimmunology
000257344 773__ $$0PERI:(DE-600)2020528-4$$a10.1111/jnc.15778$$gp. jnc.15778$$n10$$p3467 - 3481$$tJournal of neurochemistry$$v168$$x0022-3042$$y2024
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