ArticleIn vitro cellular & developmental biology. Animal2023
Inhibition of perilipin 2 attenuates cerebral ischemia/reperfusion injury by blocking NLRP3 inflammasome activation both in vivo and in vitro.
Article in In vitro cellular & developmental biology. Animal, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 9 citations in OpenAlex.
- Novel VSMC-associated biomarkers in intracranial aneurysm pathogenesis: a multi-omics and machine learning study.BMC neurology · 2026Article
- Lipid droplets in central nervous system and functional profiles of brain cells containing lipid droplets in various diseases.Journal of neuroinflammation · 2025Review
- Role of Perilipins in Oxidative Stress-Implications for Cardiovascular Disease.Antioxidants (Basel, Switzerland) · 2024Review
- Altered lipid homeostasis and autophagy precipitate diffuse alveolar hemorrhage in murine lupus.Autophagy reports · 2024Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Cerebral ischemia/reperfusion (CI/R) usually causes neuroinflammation within the central nervous system, further prompting irreversible cerebral dysfunction. Perilipin 2 (Plin2), a lipid droplet protein, has been reported to exacerbate the pathological process in different diseases, including inflammatory responses. However, the role and mechanism of Plin2 in CI/R injury are unclear. In this study, the rat models of transient middle cerebral artery occlusion followed by reperfusion (tMCAO/R) were established to mimic I/R injury, and we found that Plin2 was highly expressed in the ischemic penumbra of tMCAO/R rats. The siRNA-mediated knockdown of Plin2 significantly decreased neurological deficit scores and reduced infarct areas in rats induced by I/R. Detailed investigation showed that Plin2 deficiency alleviated inflammation of tMCAO/R rats as evidenced by reduced secretion of proinflammatory factors and the blockade of NLR family pyrin domain containing 3 (NLRP3) inflammasome activation. In vitro experiments showed that Plin2 expression was upregulated in mouse microglia subjected to oxygen-glucose deprivation/reoxygenation (OGD/R). Plin2 knockdown inhibited OGD/R-induced microglia activation and the accumulation of inflammation-related factors. Taken together, this study demonstrates that lipid droplet protein Plin2 contributes to the pathologic process of CI/R damage by impacting inflammatory response and NLRP3 inflammasome activation. Thus, Plin2 may provide a new therapeutic direction for CI/R injury.
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