ArticleInternational journal of molecular sciences2022
CCL2 Inhibition of Pro-Resolving Mediators Potentiates Neuroinflammation in Astrocytes.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- Exploring the Expression Changes of Immune Genes in Alzheimer's Disease: A Study on ANXA1, VCAM1, and CCL2.Molecular neurobiology · 2026Article
- Chronic exercise reduces astrocytic c-Fos and CCL2 via conditioned serum and cerebrospinal fluid.Narra J · 2025Article
- Chronic IL-21 drives neuroinflammation and promotes lipid accumulation in microglia.Immunity & ageing : I & A · 2025Article
- The Therapeutic Mechanisms of Huayu Quban Capsule in Treating Acne Vulgaris Are Uncovered Through Network Pharmacology and Molecular Docking.Journal of cosmetic dermatology · 2025Article
- Astrocyte-mediated inflammatory responses in traumatic brain injury: mechanisms and potential interventions.Frontiers in immunology · 2025Review
- Review
- The Role of Atypical Chemokine Receptors in Neuroinflammation and Neurodegenerative Disorders.International journal of molecular sciences · 2023Review
- Dietary Polyphenols Decrease Chemokine Release by Human Primary Astrocytes Responding to Pro-Inflammatory Cytokines.Pharmaceutics · 2023Article
- COVID-19-induced neurological symptoms: focus on the role of metal ions.Inflammopharmacology · 2023Review
- Specialized Pro-Resolving Mediators in Neuroinflammation: Overview of Studies and Perspectives of Clinical Applications.Molecules (Basel, Switzerland) · 2022Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 2 countries.
Funding
Abstract
The chemokine CCL2 participates in multiple neuroinflammatory processes, mainly through the recruitment of glial cells. However, CCL2 has also been proven to exert different types of actions on these cells, including the modification of their response to inflammatory stimuli. In the present study we analyzed the effect of CCL2 on the resolution of inflammation in astrocytes. We observed that genetic removal of CCL2 increases the expression of the enzymes responsible for the synthesis of specialized pro-resolving mediators arachidonate 15-lipoxygenase and arachidonate 5-lipoxygenase in the brain cortex of 5xFAD mice. The expression of FPR2 receptor, known to mediate the activity of pro-resolving mediators was also increased in mice lacking CCL2.The downregulation of these proteins by CCL2 was also observed in cultured astrocytes. This suggests that CCL2 inhibition of the resolution of inflammation could facilitate the progression of neuroinflammatory processes. The production of the pro-inflammatory cytokine IL-1beta by astrocytes was analyzed, and allowed us to confirm that CCL2 potentiates the activation of astrocytes trough the inhibition of pro-resolving pathways mediated by Resolvin D1. In addition, the analysis of the expression of TNFalpha, MIP1alpha and NOS2 further confirmed CCL2 inhibition of inflammation resolution in astrocytes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.