Evidence map›Paper›PMID 21940443›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011

An autocrine neuronal interleukin-6 loop mediates chloride accumulation and NKCC1 phosphorylation in axotomized sensory neurons.

Simon Pieraut, Olivier Lucas, Sina Sangari, Chamroeun Sar, Mathieu Boudes, Carine Bouffi, Danièle Noel, Frédérique Scamps

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.6field-weighted citation impact, top 8% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

23 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
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  3. Review
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  5. Review
  6. Review
  7. Article
  8. Article
  9. Chloride - The Underrated Ion in Nociceptors.Frontiers in neuroscience · 2020
    Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. NKCC1 Activation Is Required for Myelinated Sensory Neurons Regeneration through JNK-Dependent Pathway.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    Article
  15. Article
  16. Article
  17. Review
  18. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Simon PierautInserm, U-1051, Institute for Neurosciences of Montpellier-Hôpital St Eloi, 34091 Montpellier, France.
Olivier Lucas
Sina Sangari
Chamroeun Sar
Mathieu Boudes
Carine Bouffi
Danièle Noel
Frédérique Scamps
Inserm · FRInstitute for Neurosciences of Montpellier · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The cation-chloride cotransporter NKCC1 plays a fundamental role in the central and peripheral nervous systems by setting the value of intracellular chloride concentration. Following peripheral nerve injury, NKCC1 phosphorylation-induced chloride accumulation contributes to neurite regrowth of sensory neurons. However, the molecules and signaling pathways that regulate NKCC1 activity remain to be identified. Functional analysis of cotransporter activity revealed that inhibition of endogenously produced cytokine interleukin-6 (IL-6), with anti-mouse IL-6 antibody or in IL-6⁻/⁻ mice, prevented chloride accumulation in a subset of axotomized neurons. Nerve injury upregulated the transcript and protein levels of IL-6 receptor in myelinated, TrkB-positive sensory neurons of murine lumbar dorsal root ganglia. Expression of phospho-NKCC1 was observed mainly in sensory neurons expressing IL-6 receptor and was absent from IL-6⁻/⁻ dorsal root ganglia. The use of IL-6 receptor blocking-function antibody or soluble IL-6 receptor, together with pharmacological inhibition of Janus kinase, confirmed the role of neuronal IL-6 signaling in chloride accumulation and neurite growth of a subset of axotomized sensory neurons. Cell-specific expression of interleukin-6 receptor under pathophysiological conditions is therefore a cellular response by which IL-6 contributes to nerve regeneration through neuronal NKCC1 phosphorylation and chloride accumulation.

Indexed as

AnimalsAxotomyCells, CulturedChloridesEnzyme InhibitorsFemaleGanglia, SpinalInterleukin-6Janus KinasesMiceMice, Inbred C57BLMice, KnockoutNerve RegenerationNeuritesPatch-Clamp TechniquesPhosphorylationChloridesEnzyme InhibitorsInterleukin-6Janus KinasesReceptors, Interleukin-6Slc12a2 protein, mouseSodium-Potassium-Chloride SymportersSolute Carrier Family 12, Member 2

Identifiers

PMID21940443
PMCPMC6623307
OpenAlexW2021012152

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.