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Status |
Public on Apr 01, 2022 |
Title |
addition of proteasome inhibitor to J774 cells |
Organism |
Mus musculus |
Experiment type |
Expression profiling by array
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Summary |
J774 cells were treated with MG132, epoxomicin and ONX-0912 for 4 hours, and gene expression was evaluated In order to evaluate the molecular mechanism of inflammatory responses in PRAAS(Proteasome-Associated Autoinflammatory Syndromes ), we established Psmb8-KI mouse that harbors the same mutation in human patients. Psmb8-KI mice showed higher susceptibility to imiquimod-induced skin inflammation (IMS). DNA microarray analysis showed that treatment of J774 cells with proteasome inhibitors increased the expression of the Cxcl9 and Cxcl10 genes, and the skins where imiquimod was painted also expressed both genes at higher levels in Psmb8-KI than control mice. Deficiency in Cxcr3, the gene encoding the receptor of CXCL9 and CXCL10, in wild-type mice did not change IMS susceptibility, while deficiency in Cxcr3 in Psmb8-KI mice ameliorated IMS.
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Overall design |
Blockade of the CXCR3-CXCL10 axis ameliorates inflammation caused by immunoproteasome dysfunction
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Contributor(s) |
Sasaki Y, Yasutomo K |
Citation(s) |
35393946 |
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Submission date |
Nov 22, 2021 |
Last update date |
May 10, 2022 |
Contact name |
Yuki Sasaki |
E-mail(s) |
sasaki.yuki.tokushima@gmail.com
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Phone |
81-088-633-7077
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Organization name |
Tokushima University Graduate school of Medicine
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Department |
Department of Immunology and Parasitology
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Street address |
3-18-15 Kuramoto-cho
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City |
Tokushima |
ZIP/Postal code |
770-8503 |
Country |
Japan |
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Platforms (1) |
GPL11202 |
Agilent-026655 Whole Mouse Genome Microarray 4x44K v2 (Probe Name version) |
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Samples (4)
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Relations |
BioProject |
PRJNA782498 |