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Therapeutic effects of telomerase-derived peptide GV1001 in experimental autoimmune encephalomyelitis: inhibiting neuroinflammation and promoting remyelination

ABSTRACT: GV1001, a peptide derived from human telomerase reverse transcriptase, exhibits anti-cancer and anti-inflammatory actions, yet its impact on experimental autoimmune encephalomyelitis (EAE)—an established mouse model of multiple sclerosis—remains unknown. This study assessed the therapeutic potential and mechanism of GV1001 in EAE. Subcutaneous administration of GV1001 reduced clinical scores, inflammatory cytokine transcripts, and spinal cord pathology in EAE mice. Spinal cord RNA-seq showed that GV1001 suppressed immune and neuroinflammatory genes, particularly in microglia. Experiments in cultured mouse and human glia cells identified microglia as the principal cellular target. Mechanistically, GV1001 increased the NF-κB antagonist PRMT1 and boosted microglial insulin-like growth factor-1, promoting oligodendrocyte progenitor cell survival and maturation. Co-culture assays confirmed that GV1001 blunts microglial neurotoxicity and facilitates remyelination during inflammation. Collectively, the data indicate that GV1001 modulates microglial activity to attenuate neuroinflammation and foster spinal cord repair, underscoring its promise as a multitarget therapy for inflammatory demyelinating diseases such as multiple sclerosis.

ORGANISM(S): Mus musculus

PROVIDER: GSE304238 | GEO | 2025/12/01

REPOSITORIES: GEO

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Project description:Multiple sclerosis (MS) is a chronic, inflammatory, and demyelinating disease of the central nervous system (CNS). Ursolic acid (UA) can be used in the MS treatment with anti-inflammatory and neuroprotective activities. However, UA is insoluble in water, which may affect its medication effectiveness. In this study, we evaluated the pharmacological effects of UAOS-Na, a water-soluble UA derivative, on experimental autoimmune encephalomyelitis (EAE) mouse, explored its underlying mechanism, and verified the mechanism by in vitro and in vivo experiments. As we expected, UAOS-Na (30 mg/kg/d) delayed the onset time of EAE from 11.78 days post immunization (dpi) to 14.33 dpi, reduced the incidence from 90.0% to 42.9%, and was more effective than UA. UAOS-Na (60 mg/kg/d) significantly decreased the serum levels of IFN-γ, IL-17A, TNF-α and IL-6, reduced the mononuclear cell infiltration of spinal cord, and inhibited the overexpression of key transcription factors T-bet and ROR-γt of EAE mouse spinal cord and spleen. In addition, UAOS-Na attenuated demyelination and astrogliosis in the CNS of EAE and Cuprizone-induced mice. Mechanically, proteomics showed that 217 differential expression proteins (DEPs) were enriched and 215 were upregulated in EAE mice. After UAOS-Na treatment, 52 DEPs were enriched and 49 were downregulated, and these DEPs were markedly enriched in inositol phosphate metabolism, calcium, sphingolipid, cAMP, and antigen processing and presentation (APP) signaling pathways. Among them, there were few studies on APP signaling pathway related with MS. Therefore, we further investigated the effect of UAOS-Na on APP signaling pathway and found that UAOS-Na downregulated the protein levels of Tapbp and H2-T23 in MHC-I antigen presentation pathway and decreased the proliferation of splenic CD8 T cells, thereby inhibiting the CNS infiltration of CD8 T cells. Together, our findings demonstrated that UAOS-Na have both direct anti-demyelination and anti-inflammation effects. And it could reduce the inflammation of MS by downregulating the expression of Tapbp and H2-T23 in the MHC-I antigen presentation pathway.

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Therapeutic effects of telomerase-derived peptide GV1001 in experimental autoimmune encephalomyelitis: inhibiting neuroinflammation and promoting remyelination

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