ArticleCell & bioscience2021
Involvement of HECTD1 in LPS-induced astrocyte activation via σ-1R-JNK/p38-FOXJ2 axis.
Article in Cell & bioscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- HECT ubiquitin ligases as regulators of inflammatory signalling.Cell death and differentiation · 2026Review
- Role of microRNAs in major brain diseases, focusing on neuroinflammation and neuronal apoptosis.Iranian journal of basic medical sciences · 2026Review
- Sequence variants in HECTD1 result in a variable neurodevelopmental disorder.American journal of human genetics · 2025Article
- Role of ginsenoside Rb1 in attenuating depression-like symptoms through astrocytic and microglial complement C3 pathway.Metabolic brain disease · 2024Article
- Dorsal root ganglion-derived exosomes deteriorate neuropathic pain by activating microglia via the microRNA-16-5p/HECTD1/HSP90 axis.Biological research · 2024Article
- Engagement ofActa pharmaceutica Sinica. B · 2024Article
- Identification and Functional Analysis of Rare HECTD1 Missense Variants in Human Neural Tube Defects.Research square · 2024Article
- Circ-Bnc2 alleviates neuroinflammation in LPS-stimulated microglial cells to inhibit neuron cell apoptosis through regulating miR-497a-5p/HECTD1 axis.Brain and behavior · 2023Article
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundAstrocytes participate in innate inflammatory responses within the mammalian central nervous system (CNS). HECT domain E3 ubiquitin protein ligase 1 (HECTD1) functions during microglial activation, suggesting a connection with neuroinflammation. However, the potential role of HECTD1 in astrocytes remains largely unknown.
resultsHere, we demonstrated that HECTD1 was upregulated in primary mouse astrocytes after 100 ng/ml lipopolysaccharide (LPS) treatment. Genetic knockdown of HECTD1 in vitro or astrocyte-specific knockdown of HECTD1 in vivo suppressed LPS-induced astrocyte activation, whereas overexpression of HECTD1 in vitro facilitated LPS-induced astrocyte activation. Mechanistically, we established that LPS activated σ-1R-JNK/p38 pathway, and σ-1R antagonist BD1047, JNK inhibitor SP600125, or p38 inhibitor SB203580 reversed LPS-induced expression of HECTD1, thus restored LPS-induced astrocyte activation. In addition, FOXJ2 functioned as a transcription factor of HECTD1, and pretreatment of primary mouse astrocytes with BD1047, SB203580, and SP600125 significantly inhibited LPS-mediated translocation of FOXJ2 into the nucleus.
conclusionsOverall, our present findings suggest that HECTD1 participates in LPS-induced astrocyte activation by activation of σ-1R-JNK/p38-FOXJ2 pathway and provide a potential therapeutic strategy for neuroinflammation induced by LPS or any other neuroinflammatory disorders.
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