Evidence map›Paper›PMID 20109536›Full record

ReviewNeuroscience2010

Aquaporins in spinal cord injury: the janus face of aquaporin 4.

O Nesic, J D Guest, D Zivadinovic, P A Narayana, J J Herrera, R J Grill, V U L Mokkapati, B B Gelman, J Lee

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

30 citing papers in PubMed, 58 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. The potential roles of aquaporin 4 in amyotrophic lateral sclerosis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2019
    Review
  12. Article
  13. Review
  14. Neuropathic Pain After Spinal Cord Injury: Challenges and Research Perspectives.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2018
    Review
  15. Article
  16. Article
  17. Article
  18. Increased intrathecal pressure after traumatic spinal cord injury: an illustrative case presentation and a review of the literature.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2017
    Review
  19. Aquaporins in the Spinal Cord.International journal of molecular sciences · 2016
    Review
  20. Article
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

9 authors at 3 institutions in 1 country.

O NesicDepartment of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, TX, USA. Olnesic@utmb.edu
J D Guest
D Zivadinovic
P A Narayana
J J Herrera
R J Grill
V U L Mokkapati
B B Gelman
J Lee
The University of Texas Medical Branch at Galveston · USThe University of Texas Health Science Center at Houston · USUniversity of Miami · US

Funding

Aquaporins and Neuropathic Pain after Spinal Cord InjuryR21NS058417 · NINDS · UNIVERSITY OF TEXAS MED BR GALVESTON · PI NESIC-TAYLOR, OLIVERA · 2008 to 2009
$483k
NINDS NIH HHS NS05417NINDS NIH HHS R21 NS058417
6 · The paper itself

Abstract

Although malfunction of spinal cord water channels (aquaporins, AQP) likely contributes to severe disturbances in ion/water homeostasis after spinal cord injury (SCI), their roles are still poorly understood. Here we report and discuss the potential significance of changes in the AQP4 expression in human SCI that generates glial fibrillary acidic protein (GFAP)-labeled astrocytes devoid of AQP4, and GFAP-labeled astroglia that overexpress AQP4. We used a rat model of contusion SCI to study observed changes in human SCI. AQP4-negative astrocytes are likely generated during the process of SCI-induced replacement of lost astrocytes, but their origin and role in SCI remains to be investigated. We found that AQP4-overexpression is likely triggered by hypoxia. Our transcriptional profiling of injured rat cords suggests that elevated AQP4-mediated water influx accompanies increased uptake of chloride and potassium ions which represents a protective astrocytic reaction to hypoxia. However, unbalanced water intake also results in astrocytic swelling that can contribute to motor impairment, but likely only in milder injuries. In severe rat SCI, a low abundance of AQP4-overexpressing astrocytes was found during the motor recovery phase. Our results suggest that severe rat contusion SCI is a better model to analyze AQP4 functions after SCI. We found that AQP4 increases in the chronic post-injury phase are associated with the development of pain-like behavior in SCI rats, while possible mechanisms underlying pain development may involve astrocytic swelling-induced glutamate release. In contrast, the formation and size of fluid-filled cavities occurring later after SCI does not appear to be affected by the extent of increased AQP4 levels. Therefore, the effect of therapeutic interventions targeting AQP4 will depend not only on the time interval after SCI or animal models, but also on the balance between protective role of increased AQP4 in hypoxia and deleterious effects of ongoing astrocytic swelling.

Indexed as

AnimalsAquaporin 4AstrocytesDisease Models, AnimalHumansRatsSpinal CordSpinal Cord InjuriesAQP4 protein, humanAqp4 protein, ratAquaporin 4

Identifiers

PMID20109536
PMCPMC2885549
OpenAlexW1989591252

What OpenQuestion holds

Textmetadata
LicenceTDM
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 OpenQuestion graph.