ArticleJournal of neuroinflammation2013
Poly(ADP-ribose) polymerase 2 contributes to neuroinflammation and neurological dysfunction in mouse experimental autoimmune encephalomyelitis.
Article in Journal of neuroinflammation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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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.
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Who cites it
21 citing papers in PubMed, 30 citations in OpenAlex.
- PARP7 alleviates lipopolysaccharide-induced acute kidney injury by inhibiting TBK1-driven inflammation in renal tubular epithelial cells.Molecular medicine (Cambridge, Mass.) · 2026Article
- PARPs and PARP inhibitors: molecular mechanisms and clinical applications.Molecular biomedicine · 2025Review
- Review
- Specific and shared biological functions of PARP2 - is PARP2 really a lil' brother of PARP1?Expert reviews in molecular medicine · 2024Review
- PARP2 promotes inflammation in psoriasis by modulating estradiol biosynthesis in keratinocytes.Journal of molecular medicine (Berlin, Germany) · 2023Article
- PARP2 downregulation in T cells ameliorates lipopolysaccharide-induced inflammation of the large intestine.Frontiers in immunology · 2023Article
- Therapeutic Potentials of Poly (ADP-Ribose) Polymerase 1 (PARP1) Inhibition in Multiple Sclerosis and Animal Models: Concept Revisiting.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Review
- Depletion of PARP10 inhibits the growth and metastatic potential of oral squamous cell carcinoma.Frontiers in genetics · 2022Article
- PARP1-mediated PARylation activity is essential for oligodendroglial differentiation and CNS myelination.Cell reports · 2021Article
- Review
- The PARP Enzyme Family and the Hallmarks of Cancer Part 2: Hallmarks Related to Cancer Host Interactions.Cancers · 2021Review
- Article
- Poly(ADP-ribose) polymerase inhibition: past, present and future.Nature reviews. Drug discovery · 2020Review
- High RPS3A expression correlates with low tumor immune cell infiltration and unfavorable prognosis in hepatocellular carcinoma patients.American journal of cancer research · 2020Article
- The Role of PARPs in Inflammation-and Metabolic-Related Diseases: Molecular Mechanisms and Beyond.Cells · 2019Review
- Novel insights into PARPs in gene expression: regulation of RNA metabolism.Cellular and molecular life sciences : CMLS · 2019Review
- Opportunities for the repurposing of PARP inhibitors for the therapy of non-oncological diseases.British journal of pharmacology · 2018Review
- Microglial activation induced by the alarmin S100B is regulated by poly(ADP-ribose) polymerase-1.Glia · 2016Article
- Understanding specific functions of PARP-2: new lessons for cancer therapy.American journal of cancer research · 2016Review
- New facets in the regulation of gene expression by ADP-ribosylation and poly(ADP-ribose) polymerases.Chemical reviews · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundExperimental autoimmune encephalomyelitis (EAE) is an animal model of multiple sclerosis characterized by entry of activated T cells and antigen presenting cells into the central nervous system and subsequent autoimmune destruction of nerve myelin. Previous studies revealed that non-selective inhibition of poly(ADP-ribose) polymerases (PARPs) 1 and 2 protect against neuroinflammation and motor dysfunction associated with EAE, but the role of the PARP-2 isoform has not yet been investigated selectively.
resultsEAE was induced in mice lacking PARP-2, and neurological EAE signs, blood-spine barrier (BSB) permeability, demyelination and inflammatory infiltration were monitored for 35 days after immunization. Mice lacking PARP-2 exhibited significantly reduced overall disease burden and peak neurological dysfunction. PARP-2 deletion also significantly delayed EAE onset and reduced BSB permeability, demyelination and central nervous system (CNS) markers of proinflammatory Th1 and Th17 T helper lymphocytes.
conclusionsThis study represents the first description of a significant role for PARP-2 in neuroinflammation and neurological dysfunction in EAE.
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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 OpenQuestion graph.