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http://purl.uniprot.org/citations/37971567http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/37971567http://www.w3.org/2000/01/rdf-schema#comment"

Background

Recent reports suggest that peroxisome proliferator-activated receptor-γ (PPAR-γ) could promote microglial M2 polarization to inhibit inflammation. However, the specific molecular mechanisms that trigger PPAR-γ's anti-inflammatory ability in microglia are yet to be expounded. Thus, in this study, we aimed to explore the molecular mechanisms behind the anti-inflammatory effects of PPAR-γ in hypoxia-stimulated rat retinal microglial cells.

Methods and results

We used shRNA expressing lentivirus to knock down PPAR-γ and CD200 genes, and we assessed hypoxia-induced polarization markers release - M1 (iNOS, IL-1β, IL-6, and TNF-α) and M2 (Arg-1, YM1, IL-4, and IL-10) by RT-PCR. We also monitored PPAR-γ-related signals (PPAR-γ, PPAR-γ in cytoplasm or nucleus, CD200, and CD200Rs) by Western blot and RT-PCR. Our results showed that hypoxia enhanced PPAR-γ and CD200 expressions in microglial cells. Moreover, PPAR-γ agonist 15d-PGJ2 elevated CD200 and CD200R1 expressions, whereas sh-PPAR-γ had the opposite effect. Following hypoxia, expressions of M1 markers increased significantly, while those of M2 markers decreased, and the above effects were attenuated by 15d-PGJ2. Conversely, knocking down PPAR-γ or CD200 inhibited the polarization of microglial cells to M2 phenotype.

Conclusion

Our findings demonstrated that PPAR-γ performed an anti-inflammatory function in hypoxia-stimulated microglial cells by promoting their polarization to M2 phenotype via the CD200-CD200R1 pathway."xsd:string
http://purl.uniprot.org/citations/37971567http://purl.org/dc/terms/identifier"doi:10.1007/s11033-023-08815-5"xsd:string
http://purl.uniprot.org/citations/37971567http://purl.uniprot.org/core/author"Chen L."xsd:string
http://purl.uniprot.org/citations/37971567http://purl.uniprot.org/core/author"Chen C."xsd:string
http://purl.uniprot.org/citations/37971567http://purl.uniprot.org/core/author"Cui L."xsd:string
http://purl.uniprot.org/citations/37971567http://purl.uniprot.org/core/author"Hong Y."xsd:string
http://purl.uniprot.org/citations/37971567http://purl.uniprot.org/core/author"Jiang L."xsd:string
http://purl.uniprot.org/citations/37971567http://purl.uniprot.org/core/author"Li M."xsd:string
http://purl.uniprot.org/citations/37971567http://purl.uniprot.org/core/author"Zhong H."xsd:string
http://purl.uniprot.org/citations/37971567http://purl.uniprot.org/core/author"Zhang M."xsd:string
http://purl.uniprot.org/citations/37971567http://purl.uniprot.org/core/author"Xu F."xsd:string
http://purl.uniprot.org/citations/37971567http://purl.uniprot.org/core/author"Tang F."xsd:string
http://purl.uniprot.org/citations/37971567http://purl.uniprot.org/core/date"2023"xsd:gYear
http://purl.uniprot.org/citations/37971567http://purl.uniprot.org/core/name"Mol Biol Rep"xsd:string
http://purl.uniprot.org/citations/37971567http://purl.uniprot.org/core/pages"10277-10285"xsd:string
http://purl.uniprot.org/citations/37971567http://purl.uniprot.org/core/title"PPAR-gamma promotes the polarization of rat retinal microglia to M2 phenotype by regulating the expression of CD200-CD200R1 under hypoxia."xsd:string
http://purl.uniprot.org/citations/37971567http://purl.uniprot.org/core/volume"50"xsd:string
http://purl.uniprot.org/citations/37971567http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/37971567
http://purl.uniprot.org/citations/37971567http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/37971567
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