ArticleThe Journal of biological chemistry2013
HMGB1 protein does not mediate the inflammatory response in spontaneous spinal cord regeneration: a hint for CNS regeneration.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed, 48 citations in OpenAlex.
- Injection of BMSCs into the tail vertebrae vein of mice promotes spinal cord repair by inhibiting the HMGB1/RAGE signaling pathway after acute contusive spinal cord injury.In vitro cellular & developmental biology. Animal · 2025Article
- Schwann Cells and Their Exosomes: Research Progress and Prospect in Spinal Cord Injury.Neural plasticity · 2025Review
- Super-high procoagulant activity of gecko thrombin: A gift from sky dragon.CNS neuroscience & therapeutics · 2023Article
- Thrombin induces morphological and inflammatory astrocytic responses via activation of PAR1 receptor.Cell death discovery · 2022Article
- Self-Control of Inflammation during Tail Regeneration of Lizards.Journal of developmental biology · 2021Review
- Inhibiting HMGB1-RAGE axis prevents pro-inflammatory macrophages/microglia polarization and affords neuroprotection after spinal cord injury.Journal of neuroinflammation · 2020Article
- SOCS3 Attenuates GM-CSF/IFN-γ-Mediated Inflammation During Spontaneous Spinal Cord Regeneration.Neuroscience bulletin · 2020Article
- Integrated Analysis of the Mechanisms of Da-Chai-Hu Decoction in Type 2 Diabetes Mellitus by a Network Pharmacology Approach.Evidence-based complementary and alternative medicine : eCAM · 2020Article
- PGE2 facilitates tail regeneration via activation of Wnt signaling in Gekko japonicus.Journal of molecular histology · 2019Article
- Proteomics analysis of Schwann cell-derived exosomes: a novel therapeutic strategy for central nervous system injury.Molecular and cellular biochemistry · 2019Article
- High mobility group box-1 (HMGB1) is increased in injured mouse spinal cord and can elicit neurotoxic inflammation.Brain, behavior, and immunity · 2018Article
- Receptor for Advanced Glycation End-Products (RAGE) Blockade Do Damage to Neuronal Survival via Disrupting Wnt/β-Catenin Signaling in Spinal Cord Injury.Neurochemical research · 2018Article
- HMGB1 promotes ductular reaction and tumorigenesis in autophagy-deficient livers.The Journal of clinical investigation · 2018Article
- HMGB1/Advanced Glycation End Products (RAGE) does not aggravate inflammation but promote endogenous neural stem cells differentiation in spinal cord injury.Scientific reports · 2017Article
- Autologous serum supplement favours in vitro regenerative paracrine factors synthesis.Cell proliferation · 2017Article
- High-mobility group box-1 as an autocrine trophic factor in white matter stroke.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Potential Involvement of Snail Members in Neuronal Survival and Astrocytic Migration during the Gecko Spinal Cord Regeneration.Frontiers in cellular neuroscience · 2017Article
- Reactive oxygen species generated from skeletal muscles are required for gecko tail regeneration.Scientific reports · 2016Article
- Old dogs with new tricks: intra-axonal translation of nuclear proteins.Neural regeneration research · 2015Article
- The HMGB1 signaling pathway activates the inflammatory response in Schwann cells.Neural regeneration research · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Uncontrolled, excessive inflammation contributes to the secondary tissue damage of traumatic spinal cord, and HMGB1 is highlighted for initiation of a vicious self-propagating inflammatory circle by release from necrotic cells or immune cells. Several regenerative-competent vertebrates have evolved to circumvent the second damages during the spontaneous spinal cord regeneration with an unknown HMGB1 regulatory mechanism. By genomic surveys, we have revealed that two paralogs of HMGB1 are broadly retained from fish in the phylogeny. However, their spatial-temporal expression and effects, as shown in lowest amniote gecko, were tightly controlled in order that limited inflammation was produced in spontaneous regeneration. Two paralogs from gecko HMGB1 (gHMGB1) yielded distinct injury and infectious responses, with gHMGB1b significantly up-regulated in the injured cord. The intracellular gHMGB1b induced less release of inflammatory cytokines than gHMGB1a in macrophages, and the effects could be shifted by exchanging one amino acid in the inflammatory domain. Both intracellular proteins were able to mediate neuronal programmed apoptosis, which has been indicated to produce negligible inflammatory responses. In vivo studies demonstrated that the extracellular proteins could not trigger a cascade of the inflammatory cytokines in the injured spinal cord. Signal transduction analysis found that gHMGB1 proteins could not bind with cell surface receptors TLR2 and TLR4 to activate inflammatory signaling pathway. However, they were able to interact with the receptor for advanced glycation end products to potentiate oligodendrocyte migration by activation of both NFκB and Rac1/Cdc42 signaling. Our results reveal that HMGB1 does not mediate the inflammatory response in spontaneous spinal cord regeneration, but it promotes CNS regeneration.
Indexed as
Identifiers
What OpenQuestion holds
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 OpenQuestion graph.