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Cited by 6Neuroinflammation and Neurodegeneration MechanismsCholesterol and Lipid MetabolismInflammation biomarkers and pathways

Potential role of TREM2 in high cholesterol-induced cell injury and metabolic dysfunction in SH-SY5Y cells

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Zheng, Qiang, Han, Yinxiu, Fan, Min, Gao, Xinran, Ma, Mengdie, Xu, Jingxian, Liu, Sen, Ge, Jinfang·2023·Experimental and Therapeutic Medicine
DOI 10.3892/etm.2023.11904PMC PMC10119670
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Abstract

Triggering receptor expressed on myeloid cells 2 (TREM2) is an important member of the immunoglobulin family of inflammatory stimulating receptors and is involved in a number of pathophysiological processes. The present study aimed to investigate the role of TREM2 in neurotoxicity induced by high cholesterol levels in SH-SY5Y cells and explore the potential mechanism. SH-SY5Y cells were routinely cultured and stimulated with a range of cholesterol concentrations. Cell viability was assessed using an MTT assay, morphological changes were observed, and the cell cycle distribution was measured using flow cytometry. Lipid deposition was measured by Oil red O staining, and the mRNA and protein expression levels of SRBEP-1 and SRBEP-2 were detected by quantitative PCR and western blotting, respectively. Moreover, the protein expression levels of BDNF, Copine-6, TREM1, TREM2, and key molecules of the Wnt signaling pathways were detected by western blotting. Finally, TREM2 was overexpressed to investigate its potential role in high cholesterol-induced neurotoxicity. The results showed that cell viability was significantly decreased in SH-SY5Y cells stimulated with cholesterol (0.1~100 µM) in a dose- and time-dependent manner. Stimulation with 100 µM cholesterol for 24 h resulted in morphological injuries, increased the proportion of SH-SY5Y cells at G0/G1, the degree of lipid accumulation, and the protein expression levels of sterol regulatory element binding protein (SREBP)1 and SREBP2, markedly decreased the protein expression levels of BDNF, Copine-6, and TREM2, and the p-β-catenin/β-catenin ratio, and increased the expression levels of nesfatin-1, TREM1 and the p-GSK3β/GSK3β ratio. Furthermore, the imbalanced expression of BDNF, Copine-6, nesfatin-1, and p-GSK3β induced by high cholesterol levels was reversed after overexpression of TREM2. These results suggest that a high concentration of cholesterol could induce cell injury and lipid deposition in SH-SY5Y cells and that the underlying mechanism may be associated with imbalanced TREM2 expression.

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  • Imbalance of TREM2 expression is involved in neuronal injury induced by high cholesterol and is related to LPS-induced hyperactivation of microglia and increased secretion of inflammatory factors.

    “The results of our previous studies showed that the imbalance of TREM2 expression was not only involved in the process of neuronal injury induced by high cholesterol but also related to LPS-induced hyperactivation of microglia and increased secretion of inflammatory factors (X. R. Gao et al., 2021; Liu et al., 2022; Zheng et al., 2023).”

    From AD-Like Neuropsychiatric Dysfunction in a Mice Model Induced by a Combination of High-Fat Diet and Intraperitoneal Injection of Streptozotocin (2024) · cites this paper as Zheng et al., 2023

    The Discussion (page not provided) reports that high cholesterol injured SH-SY5Y cells, decreased TREM2 expression, and that TREM2 may play a role in those injuries. It does not report LPS-induced microglial hyperactivation or increased secretion of inflammatory factors, so it supports only the cholesterol-injury part of the jointly cited sentence. (LLM, conf=0.88)

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  • Imbalance of TREM2 is involved in neuronal injury induced by high cholesterol and is related to LPS-induced homeostatic imbalance of microglia and increased secretion of inflammatory factors.

    “The results of our previous studies showed that the imbalance expression of TREM2 was not only involved in the neuronal injury induced by high cholesterol but also related to LPS-induced homeostatic imbalance of microglia and increased secretion of inflammatory factors (Liu et al., 2022; Zheng et al., 2023).”

    From AD-Like Neuropsychiatric Dysfunction in a Mice Model Induced by a Combination of High-Fat Diet and Intraperitoneal Injection of Streptozotocin (2024) · cites this paper as Zheng et al., 2023

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Cited by

Sorted by citations

Authors
Zheng, Q., Han, Y., Fan, M., Gao, X., Ma, M., Xu, J., Liu, S., & Ge, J.
Affiliations
  • Anhui Medical University (CN)
  • School of Pharmacy, Anhui Medical University, Hefei, Anhui 230032, P.R. China
ORCID
Venue
Experimental and Therapeutic Medicine
Publisher
Spandidos Publications
Published
2023-03-22
Volume
25
Issue
5
Pages
205-205
ISSN
  • 1792-0981 (ISSN-L)
  • 1792-1015
DOI
10.3892/etm.2023.11904
PMC
PMC10119670
OpenAlex
W4353090864
Cited by
6
References
9
Citations by year
2026: 1 · 2025: 2 · 2024: 2 · 2023: 1
FWCI
0.62
Type
journal article
Language
en
Open access
Licence
cc-by-nc-nd
Locations
  • Experimental and Therapeutic Medicine (publishedVersion, cc-by-nc-nd)
  • PubMed Central (publishedVersion, cc-by-nc-nd)
  • PubMed (publishedVersion)
Funders
  • National Natural Science Foundation of China (81701327, 81870403)
  • Anhui Medical University (2022xkjT009)
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
  • Life Sciences › Immunology and Microbiology › Immunology › Inflammation biomarkers and pathways
Keywords
TREM2, hypercholesterolemia, neurotoxicity, SH-SY5Y cells, SREBP1, SREBP2, lipid accumulation, Wnt signaling, GSK3β, brain-derived neurotrophic factor, nesfatin-1, TREM-1, cell cycle arrest, neuroinflammation

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