ArticleMolecular neurobiology2016
Aldose Reductase Regulates Microglia/Macrophages Polarization Through the cAMP Response Element-Binding Protein After Spinal Cord Injury in Mice.
Article in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 64 citations in OpenAlex.
- Xanthoxylin Regulating the Inflammatory Microenvironment After Spinal Cord Injury Through Inhibition of the NF-κB Signaling Pathway.Neuromolecular medicine · 2025Article
- HPGD: An Intermediate Player in Microglial Polarization and Multiple Sclerosis Regulated by Nr4a1.Molecular neurobiology · 2025Article
- The Roles of RhoA/ROCK/NF-κB Pathway in Microglia Polarization Following Ischemic Stroke.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2024Review
- Temporal changes of spinal microglia in murine models of neuropathic pain: a scoping review.Frontiers in immunology · 2024Article
- The Aldose Reductase Inhibitor Epalrestat Maintains Blood-Brain Barrier Integrity by Enhancing Endothelial Cell Function during Cerebral Ischemia.Molecular neurobiology · 2023Article
- Potential regulatory effects of stem cell exosomes on inflammatory response in ischemic stroke treatment.World journal of stem cells · 2023Review
- IL1RAP Knockdown in LPS-Stimulated Normal Human Astrocytes Suppresses LPS-Induced Reactive Astrogliosis and Promotes Neuronal Cell Proliferation.Neurochemical research · 2023Article
- Metabolic Reprogramming of Microglia in Sepsis-Associated Encephalopathy: Insights from Neuroinflammation.Current neuropharmacology · 2023Review
- The Role of Aldose Reductase in Beta-Amyloid-Induced Microglia Activation.International journal of molecular sciences · 2022Article
- Reducing host aldose reductase activity promotes neuronal differentiation of transplanted neural stem cells at spinal cord injury sites and facilitates locomotion recovery.Neural regeneration research · 2022Article
- Blood-Spinal Cord Barrier: Its Role in Spinal Disorders and Emerging Therapeutic Strategies.NeuroSci · 2022Review
- Activation of Three Major Signaling Pathways After Endurance Training and Spinal Cord Injury.Molecular neurobiology · 2022Article
- Microglia Polarization From M1 to M2 in Neurodegenerative Diseases.Frontiers in aging neuroscience · 2022Review
- Glial-Neuronal Interactions in Pathogenesis and Treatment of Spinal Cord Injury.International journal of molecular sciences · 2021Review
- Gramine promotes functional recovery after spinal cord injury via ameliorating microglia activation.Journal of cellular and molecular medicine · 2021Article
- Aldose reductase deficiency inhibits LPS-induced M1 response in macrophages by activating autophagy.Cell & bioscience · 2021Article
- Mitochondria-Targeted Therapeutics for Alzheimer's Disease: The Good, the Bad, the Potential.Antioxidants & redox signaling · 2021Review
- Microglia-Mediated Neurodegeneration in Perinatal Brain Injuries.Biomolecules · 2021Review
- Role of the Polyol Pathway in Locomotor Recovery and Wallerian Degeneration after Spinal Cord Contusion Injury.Neurotrauma reports · 2021Article
- Platelet-rich plasma improves chronic inflammatory pain by inhibiting PKM2-mediated aerobic glycolysis in astrocytes.Annals of translational medicine · 2020Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammatory reactions are the most critical pathological processes occurring after spinal cord injury (SCI). Activated microglia/macrophages have either detrimental or beneficial effects on neural regeneration based on their functional polarized M1/M2 subsets. However, the mechanism of microglia/macrophage polarization to M1/M2 at the injured spinal cord environment remains unknown. In this study, wild-type (WT) or aldose reductase (AR)-knockout (KO) mice were subjected to SCI by a spinal crush injury model. The expression pattern of AR, behavior tests for locomotor activity, and lesion size were assessed at between 4 h and 28 days after SCI. We found that the expression of AR is upregulated in microglia/macrophages after SCI in WT mice. In AR KO mice, SCI led to smaller injury lesion areas compared to WT. AR deficiency-induced microglia/macrophages induce the M2 rather than the M1 response and promote locomotion recovery after SCI in mice. In the in vitro experiments, microglia cell lines (N9 or BV2) were treated with the AR inhibitor (ARI) fidarestat. AR inhibition caused 4-hydroxynonenal (HNE) accumulation, which induced the phosphorylation of the cAMP response element-binding protein (CREB) to promote Arg1 expression. KG501, the specific inhibitor of phosphorylated CREB, could cancel the upregulation of Arg1 by ARI or HNE stimulation. Our results suggest that AR works as a switch which can regulate microglia by polarizing cells to either the M1 or the M2 phenotype under M1 stimulation based on its states of activity. We suggest that inhibiting AR may be a promising therapeutic method for SCI in the future.
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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 OpenQuestion graph.