ArticleInflammopharmacology2016
IL-17 induces MIP-1α expression in primary mouse astrocytes via TRPC channel.
Article in Inflammopharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Causal Effects of Inflammatory Cytokines on Bipolar Disorder: A Bidirectional Two-Sample Mendelian Randomization Study.Brain and behavior · 2025Article
- Multi-omics association study integrating GWAS and pQTL data revealed MIP-1α as a potential drug target for erectile dysfunction.Frontiers in pharmacology · 2024Article
- Tumor-Derived Autophagosomes (DRibbles) Activate Human B Cells to Induce Efficient Antigen-Specific Human Memory T-Cell Responses.Frontiers in immunology · 2021Article
- Maternal IL-17A in autism.Experimental neurology · 2018Review
- Inhibiting Interleukin 17 Can Ameliorate the Demyelination Caused byMediators of inflammation · 2017Article
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Authors and funding
7 authors.
Funding
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Abstract
Our previous study demonstrated IL-17-mediated induction of MIP-1α through its binding to the cognate IL-17RA and MIP-1α was involved in astrocyte activation. Transient receptor potential canonical (TRPC) channel was involved in astrocyte activation, however, whether TRPC channel regulates MIP-1α expression in the context of multiple sclerosis (MS) remains largely unknown. In this study we identify the essential role of TRPC channel in IL-17-mediated MIP-1α expression and astrocyte activation. Moreover, treatment of astrocytes with IL-17 activated MAPKs and PI3K/Akt signaling pathways with downstream NF-κB pathways. Interestingly, the TRPC blocker-SKF96365 (10 μM) and Norgestimate (10 μM) significantly inhibited the increased expression of MIP-1α via suppression of IL-17-mediated ERK, p38 and JNK MAPKs and PI3K/Akt pathway activation, thereby underscoring the role of TRPC channel in this process. Together these data underpin the role of TRPC channel as a novel target that regulates MIP-1α expression and cell activation-mediated by IL-17 with implications for therapeutic intervention for reversal of neuroinflammation inflicted by IL-17. Understanding the regulation of MIP-1α expression may provide insights into the development of potential therapeutic targets for neuroinflammation associated with MS.
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