Evidence map›Paper›PMID 24148248›Full record

ArticleBiochemical and biophysical research communications2013

Aquaporin 5 knockout mouse lens develops hyperglycemic cataract.

S Sindhu Kumari, Kulandaiappan Varadaraj

Open access · greenAbstract read
In one paragraph

Article in Biochemical and biophysical research communications, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

25 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Methods for studying mammalian aquaporin biology.Biology methods & protocols · 2023
    Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Aqp0a Regulates Suture Stability in the Zebrafish Lens.Investigative ophthalmology & visual science · 2018
    Article
  16. The Role of Aquaporins in Ocular Lens Homeostasis.International journal of molecular sciences · 2017
    Review
  17. Article
  18. Role of Aquaporin 0 in lens biomechanics.Biochemical and biophysical research communications · 2015
    Article
  19. Article
  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

2 authors at 1 institution in 1 country.

S Sindhu KumariDepartment of Physiology and Biophysics, Stony Brook University, Stony Brook, NY 11794-8661, United States.
Kulandaiappan Varadaraj
Stony Brook University · US

Funding

Role of Aquaporin-0 for cell-to-cell adhesion and lens transparencyR01EY020506 · NEI · STATE UNIVERSITY NEW YORK STONY BROOK · PI VARADARAJ, KULANDAIAPPAN · 2010 to 2013
$1.6M
NEI NIH HHS R01 EY020506NEI NIH HHS R01 EY20506
6 · The paper itself

Abstract

The scope of this investigation was to understand the role of aquaporin 5 (AQP5) for maintaining lens transparency and homeostasis. Studies were conducted using lenses of wild-type (WT) and AQP5 knockout (AQP5-KO) mice. Immunofluorescent staining verified AQP5 expression in WT lens sections and lack of expression in the knockout. In vivo and ex vivo, AQP5-KO lenses resembled WT lenses in morphology and transparency. Therefore, we subjected the lenses ex vivo under normal (5.6mM glucose) and hyperglycemic (55.6mM glucose) conditions to test for cataract formation. Twenty-four hours after incubation in hyperglycemic culture medium, AQP5-KO lenses showed mild opacification which was accelerated several fold at 48 h; in contrast, WT lenses remained clear even after 48 h of hyperglycemic treatment. AQP5-KO lenses displayed osmotic swelling due to increase in water content. Cellular contents began to leak into the culture medium after 48 h. We reason that water influx through glucose transporters and glucose cotransporters into the cells could mainly be responsible for creating hyperglycemic osmotic swelling; absence of AQP5 in fiber cells appears to cause lack of required water efflux, challenging cell volume regulation and adding to osmotic swelling. This study reveals that AQP5 could play a critical role in lens microcirculation for maintaining transparency and homeostasis, especially by providing protection under stressful conditions. To the best of our knowledge, this is the first report providing evidence that AQP5 facilitates maintenance of lens transparency and homeostasis by regulating osmotic swelling caused by glucose transporters and cotransporters under hyperglycemic stressful conditions.

Indexed as

AnimalsAquaporin 5CataractGlucoseHyperglycemiaLens, CrystallineMiceMice, Inbred C57BLMice, KnockoutOsmotic PressureAqp5 protein, mouseAquaporin 5GlucoseAQP5GLUT1GLUT3HyperglycemiaLens cataractLens transparencySGLT1SGLT2Sodium-dependent glucose cotransportersWater channel

Identifiers

PMID24148248
PMCPMC3863611
OpenAlexW2088047910

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.