ArticleEMBO molecular medicine2013
LPS resistance of SPRET/Ei mice is mediated by Gilz, encoded by the Tsc22d3 gene on the X chromosome.
Article in EMBO molecular medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 57 citations in OpenAlex.
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- Treating the Side Effects of Exogenous Glucocorticoids; Can We Separate the Good From the Bad?Endocrine reviews · 2023Review
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- Neuroinflammatory astrocyte subtypes in the mouse brain.Nature neuroscience · 2021Article
- Glucocorticoids in Sepsis: To Be or Not to Be.Frontiers in immunology · 2020Review
- Glucocorticoid-Induced Leucine Zipper: A Promising Marker for Monitoring and Treating Sepsis.Frontiers in immunology · 2020Review
- Short-Chain Alcohols Upregulate GILZ Gene Expression and Attenuate LPS-Induced Septic Immune Response.Frontiers in immunology · 2020Article
- A General Introduction to Glucocorticoid Biology.Frontiers in immunology · 2019Review
- Glucocorticoid-Induced Leucine Zipper: A Novel Anti-inflammatory Molecule.Frontiers in pharmacology · 2019Review
- Cdk5 Deletion Enhances the Anti-inflammatory Potential of GC-Mediated GR Activation During Inflammation.Frontiers in immunology · 2019Article
- Implicating the Role of GILZ in Glucocorticoid Modulation of T-Cell Activation.Frontiers in immunology · 2019Review
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Natural variation for LPS-induced lethal inflammation in mice is useful for identifying new genes that regulate sepsis, which could form the basis for novel therapies for systemic inflammation in humans. Here we report that LPS resistance of the inbred mouse strain SPRET/Ei, previously reported to depend on the glucocorticoid receptor (GR), maps to the distal region of the X-chromosome. The GR-inducible gene Tsc22d3, encoding the protein Gilz and located in the critical region on the X-chromosome, showed a higher expressed SPRET/Ei allele, regulated in cis. Higher Gilz levels were causally related to reduced inflammation, as shown with knockdown and overexpression studies in macrophages. Transient overexpression of Gilz by hydrodynamic plasmid injection confirmed that Gilz protects mice against endotoxemia Our data strongly suggest that Gilz is responsible for the LPS resistance of SPRET/Ei mice and that it could become a treatment option for sepsis.
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