Ghrelin Inhibits Oligodendrocyte Cell Death by Attenuating Microglial Activation
Open accessAbstract
BACKGROUND: Recently, we reported the antiapoptotic effect of ghrelin in spinal cord injury-induced apoptotic cell death of oligodendrocytes. However, how ghrelin inhibits oligodendrocytes apoptosis, is still unknown. Therefore, in the present study, we examined whether ghrelin inhibits microglia activation and thereby inhibits oligodendrocyte apoptosis. METHODS: Using total cell extracts prepared from BV-2 cells activated by lipopolysaccharide (LPS) with or without ghrelin, the levels of p-p38 phosphor-p38 mitogen-activated protein kinase (p-p38MAPK), phospho-c-Jun N-terminal kinase (pJNK), p-c-Jun, and pro-nerve growth factor (proNGF) were examined by Western blot analysis. Reactive oxygen species (ROS) production was investigated by using dichlorodihydrofluorescein diacetate. To examine the effect of ghrelin on oligodendrocyte cell death, oligodendrocytes were cocultured in transwell chambers of 24-well plates with LPS-stimulated BV-2 cells. After 48 hours incubation, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and terminal deoxynucleotidyl transferase 2'-deoxyuridine, 5'-triphosphate nick end labeling staining were assessed. RESULTS: Ghrelin treatment significantly decreased levels of p-p38MAPK, p-JNK, p-c-Jun, and proNGF in LPS-stimulated BV-2 cells. ROS production increased in LPS-stimulated BV-2 cells was also significantly inhibited by ghrelin treatment. In addition, ghrelin significantly inhibited oligodendrocyte cell death when cocultured with LPS-stimulated BV-2 cells. CONCLUSION: Ghrelin inhibits oligodendrocyte cell death by decreasing proNGF and ROS production as well as p38MAPK and JNK activation in activated microglia as an anti-inflammatory hormone.
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Ghrelin could affect microglia functions indirectly by modulating other brain cell types that do express GHSR, such as neurons and astrocytes.
“Hence, ghrelin could affect microglia functions indirectly by modulating other brain cell types that do express the GHSR, such as neurons [53, 54, 57] and astrocytes [58].”
From Protective PLCG2 variants associate with a delayed onset of Alzheimer’s disease among heterozygous APOE ε4 carriers (2026) · cites this paper as [53]
The Discussion reports that microglia and BV-2 cells lack GHS-R1a and that ghrelin inhibits microglial activation. It does not say that ghrelin acts indirectly through GHSR-expressing neurons or astrocytes; instead, it proposes a receptor-independent pathway in BV-2 cells and says the mechanism needs further study. (LLM, conf=0.85)
Experimental — accuracy not yet measuredGhrelin treatment suppresses inflammatory response and reduces reactive oxygen species production in microglial cells.
“Yet, ghrelin treatment has been shown to suppress inflammatory response and reduce reactive oxygen species production in microglial cells [53, 54].”
From Protective PLCG2 variants associate with a delayed onset of Alzheimer’s disease among heterozygous APOE ε4 carriers (2026) · cites this paper as [53]
Microglia lack GHSR, the primary receptor for ghrelin.
“Moreover, microglia lack the GHSR, the primary receptor for ghrelin [53–55].”
From Protective PLCG2 variants associate with a delayed onset of Alzheimer’s disease among heterozygous APOE ε4 carriers (2026) · cites this paper as [53]
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“Hence, ghrelin could affect microglia functions indirectly by modulating other brain cell types that do express the GHSR, such as neurons (52,53,56) and astrocytes (57).”
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- Authors
- Lee, J. Y., & Yune, T. Y.
- Affiliations
- Kyung Hee University (KR)
- Corresponding author
- Yune, Tae Young
- Venue
- Endocrinology and Metabolism
- Publisher
- Korean Endocrine Society
- Published
- 2014
- Volume
- 29
- Issue
- 3
- Pages
- 371
- ISSN
- 2093-596X (ISSN-L)
- 2093-5978
- PMC
- PMC4192814
- OpenAlex
- W2119547785
- Cited by
- 37
- References
- 35
- Citations by year
- 2026: 3 · 2025: 4 · 2024: 4 · 2022: 4 · 2021: 4 · 2020: 1 · 2019: 3 · 2018: 2 · 2017: 5 · 2016: 4 · 2015: 3
- FWCI
- 2.08
- Type
- journal article
- Language
- en
- Open access
- diamond
- doi.org
- Licence
- Locations
- Endocrinology and Metabolism (publishedVersion, cc-by-nc)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Korea Health Industry Development Institute
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
- Keywords
- ghrelin, oligodendrocyte apoptosis, microglial activation, reactive oxygen species, p38 MAPK, JNK, c-Jun, lipopolysaccharide, spinal cord injury, neuroprotection
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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