ArticleScientific reports2022
sTREM-1 promotes the phagocytic function of microglia to induce hippocampus damage via the PI3K-AKT signaling pathway.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 29 citations in OpenAlex.
- Soluble TREM1 Contributes to Aging-Related Neurodegeneration via ROBO2/ERK Pathway.Molecular neurobiology · 2026Article
- Application value of serum high mobility group protein B1 (HMGB1) and soluble triggering receptor-1 (sTREM-1) levels in the prognostic assessment of trauma.Journal of medical biochemistry · 2026Article
- Ionizing radiation and Alzheimer's disease: epidemiology, mechanisms, and eCIRP-mediated tau pathology.Frontiers in immunology · 2026Review
- Microglia-Mediated Neuroinflammation Through Phosphatidylinositol 3-Kinase Signaling Causes Cognitive Dysfunction.International journal of molecular sciences · 2025Review
- Astragalin-functionalized ultrasmall nanoparticles modulate the complement pathway to inhibit microglial synaptic phagocytosis for reducing anesthetic neurotoxicity.Materials today. Bio · 2025Article
- Role of triggering receptor expressed on myeloid cells 1/2 in secondary injury after cerebral hemorrhage.World journal of clinical cases · 2025Review
- Predictive Value of Urinary KIM-1, TIMP-2 and sTREM-1 for Contrast-Induced Acute Kidney Injury in Elderly Patients After Percutaneous Coronary Intervention.International journal of general medicine · 2025Article
- Reply to Pomara et al: A potential role for sTREM2 in PTSD?Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- WIF-1 contributes to lupus-induced neuropsychological deficits via the CRYAB/STAT4-SHH axis.Arthritis research & therapy · 2024Article
- Pharmacological Inhibition or Silencing of TREM1 Restrains HCC Cell Metastasis by Inactivating TLR/PI3K/AKT Signaling.Cell biochemistry and biophysics · 2024Article
- Article
- Activation of LXRs alleviates neuropathic pain-induced cognitive dysfunction by modulation of microglia polarization and synaptic plasticity via PI3K/AKT pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Article
- Microglial senescence contributes to female-biased neuroinflammation in the aging mouse hippocampus: implications for Alzheimer's disease.Journal of neuroinflammation · 2023Article
- Microglial senescence contributes to female-biased neuroinflammation in the aging mouse hippocampus: implications for Alzheimer's disease.bioRxiv : the preprint server for biology · 2023Article
- Aging alters mechanisms underlying voluntary movements in spinal motor neurons of mice, primates, and humans.JCI insight · 2023Article
- Microglia activation in the presence of intact blood-brain barrier and disruption of hippocampal neurogenesis via IL-6 and IL-18 mediate early diffuse neuropsychiatric lupus.Annals of the rheumatic diseases · 2023Article
- The role of triggering receptor expressed on myeloid cells-1 (TREM-1) in central nervous system diseases.Molecular brain · 2022Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Soluble triggering receptor expressed on myeloid cells-1 (sTREM-1) is a soluble form of TREM-1 released during inflammation. Elevated sTREM-1 levels have been found in neuropsychiatric systemic lupus erythematosus (NPSLE) patients; yet, the exact mechanisms remain unclear. This study investigated the role of sTREM-1 in brain damage and its underlying mechanism. The sTREM-1 recombinant protein (2.5 μg/3 μL) was injected into the lateral ventricle of C57BL/6 female mice. After intracerebroventricular (ICV) injection, the damage in hippocampal neurons increased, and the loss of neuronal synapses and activation of microglia increased compared to the control mice (treated with saline). In vitro. after sTREM-1 stimulation, the apoptosis of BV2 cells decreased, the polarization of BV2 cells shifted to the M1 phenotype, the phagocytic function of BV2 cells significantly improved, while the PI3K-AKT signal pathway was activated in vivo and in vitro. PI3K-AKT pathway inhibitor LY294002 reversed the excessive activation and phagocytosis of microglia caused by sTREM-1 in vivo and in vitro, which in turn improved the hippocampus damage. These results indicated that sTREM-1 activated the microglial by the PI3K-AKT signal pathway, and promoted its excessive phagocytosis of the neuronal synapse, thus inducing hippocampal damage. sTREM-1 might be a potential target for inducing brain lesions.
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