PSMC5 regulates microglial polarization and activation in LPS-induced cognitive deficits and motor impairments by interacting with TLR4 Article Swipe
Wei Bi
,
Keyao Bao
,
Xinqi Zhou
,
Yihui Deng
,
Xiaoting Li
,
Jiawei Zhang
,
Xin Lan
,
Jiayi Zhao
,
Daxiang Lu
,
Yezi Xu
,
Yanmei Cen
,
Rui Cao
,
Mengyang Xu
,
Wenbin Zhong
,
Li Zhu
·
YOU?
·
· 2023
· Open Access
·
· DOI: https://doi.org/10.1186/s12974-023-02904-9
YOU?
·
· 2023
· Open Access
·
· DOI: https://doi.org/10.1186/s12974-023-02904-9
Luteolin is a flavonoid found in high concentrations in celery and green pepper, and acts as a neuroprotectant. PSMC5 (proteasome 26S subunit, ATPase 5) protein levels were reduced after luteolin stimulation in activated microglia. We aimed to determine whether regulating PSMC5 expression could inhibit neuroinflammation, and investigate the underlying mechanisms.BV2 microglia were transfected with siRNA PSMC5 before the addition of LPS (lipopolysaccharide, 1.0 µg/ml) for 24 h in serum free DMEM. A mouse model of LPS-induced cognitive and motor impairment was established to evaluate the neuroprotective effects of shRNA PSMC5. Intracerebroventricular administration of shRNA PSMC5 was commenced 7 days prior to i.p. injection of LPS (750 μg/kg). Treatments and behavioral experiments were performed once daily for 7 consecutive days. Behavioral tests and pathological/biochemical assays were performed to evaluate LPS-induced hippocampal damage. Molecular dynamics simulation was used to confirm the interaction between PSMC5 and TLR4 (Toll-like receptor 4) in LPS-stimulated BV2 microglia. SiRNA PSMC5 inhibited BV2 microglial activation, and suppressed the release of inflammatory factors (IL-1β, COX-2, PGE 2 , TNF-α, and iNOS) upon after LPS stimulation in BV2 microglia. LPS increased IκB-α and p65 phosphorylation, which was attenuated by siRNA PSMC5. Behavioral tests and pathological/biochemical assays showed that shRNA PSMC5 attenuated LPS-induced cognitive and motor impairments, and restored synaptic ultrastructure and protein levels in mice. ShRNA PSMC5 reduced pro-inflammatory cytokine (TNF-α, IL-1β, PGE 2 , and NO) levels in the serum and brain, and relevant protein factors (iNOS and COX-2) in the brain. Furthermore, shRNA PSMC5 upregulated the anti-inflammatory mediators interleukin IL-4 and IL-10 in the serum and brain, and promoted a pro-inflammation-to-anti-inflammation phenotype shift in microglial polarization. Mechanistically, shRNA PSMC5 significantly alleviated LPS-induced TLR4 expression. The polarization of LPS-induced microglial pro-inflammation phenotype was abolished by TLR4 inhibitor and in the TLR-4 −/− mouse, as in shRNA PSMC5 treatment. PSMC5 interacted with TLR4 via the amino sites Glu284, Met139, Leu127, and Phe283. PSMC5 site mutations attenuated neuroinflammation and reduced pro-inflammatory factors by reducing TLR4-related effects, thereby reducing TLR4-mediated MyD88 (myeloid differentiation factor 88)-dependent activation of NF-κB. PSMC5 could be an important therapeutic target for treatment of neurodegenerative diseases involving neuroinflammation-associated cognitive deficits and motor impairments induced by microglial activation. Graphical Abstract
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- Type
- article
- Language
- en
- Landing Page
- https://doi.org/10.1186/s12974-023-02904-9
- https://jneuroinflammation.biomedcentral.com/counter/pdf/10.1186/s12974-023-02904-9
- OA Status
- gold
- Cited By
- 34
- References
- 54
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W4388971273
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Raw OpenAlex JSON
- OpenAlex ID
-
https://openalex.org/W4388971273Canonical identifier for this work in OpenAlex
- DOI
-
https://doi.org/10.1186/s12974-023-02904-9Digital Object Identifier
- Title
-
PSMC5 regulates microglial polarization and activation in LPS-induced cognitive deficits and motor impairments by interacting with TLR4Work title
- Type
-
articleOpenAlex work type
- Language
-
enPrimary language
- Publication year
-
2023Year of publication
- Publication date
-
2023-11-24Full publication date if available
- Authors
-
Wei Bi, Keyao Bao, Xinqi Zhou, Yihui Deng, Xiaoting Li, Jiawei Zhang, Xin Lan, Jiayi Zhao, Daxiang Lu, Yezi Xu, Yanmei Cen, Rui Cao, Mengyang Xu, Wenbin Zhong, Li ZhuList of authors in order
- Landing page
-
https://doi.org/10.1186/s12974-023-02904-9Publisher landing page
- PDF URL
-
https://jneuroinflammation.biomedcentral.com/counter/pdf/10.1186/s12974-023-02904-9Direct link to full text PDF
- Open access
-
YesWhether a free full text is available
- OA status
-
goldOpen access status per OpenAlex
- OA URL
-
https://jneuroinflammation.biomedcentral.com/counter/pdf/10.1186/s12974-023-02904-9Direct OA link when available
- Concepts
-
Microglia, Neuroinflammation, TLR4, Neuroprotection, Small hairpin RNA, Lipopolysaccharide, Pharmacology, Hippocampal formation, Chemistry, Tumor necrosis factor alpha, Medicine, Inflammation, Cell biology, Immunology, Endocrinology, Biology, Biochemistry, Gene knockdown, ApoptosisTop concepts (fields/topics) attached by OpenAlex
- Cited by
-
34Total citation count in OpenAlex
- Citations by year (recent)
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2025: 20, 2024: 14Per-year citation counts (last 5 years)
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54Number of works referenced by this work
- Related works (count)
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10Other works algorithmically related by OpenAlex
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