Evidence map›Paper›PMID 20522648›Full record

ArticleThe American journal of pathology2010

Potential down-regulation of salivary gland AQP5 by LPS via cross-coupling of NF-kappaB and p-c-Jun/c-Fos.

Chenjuan Yao, Nunuk Purwanti, Mileva Ratko Karabasil, Ahmad Azlina, Purevjav Javkhlan, Takahiro Hasegawa, Tetsuya Akamatsu, Toru Hosoi, Koichiro Ozawa, Kazuo Hosoi

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

29 citing papers in PubMed, 55 citations in OpenAlex.

  1. Organoid-based modeling and regenerative strategies for salivary gland dysfunction.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
    Review
  2. Review
  3. Aquaporin-5 Dynamic Regulation.International journal of molecular sciences · 2023
    Review
  4. Aquaporins in Glandular Secretion.Advances in experimental medicine and biology · 2023
    Article
  5. Aquaporins in Tumor.Advances in experimental medicine and biology · 2023
    Article
  6. Article
  7. Effect of Lipopolysaccharide and TNFMediators of inflammation · 2021
    Article
  8. Review
  9. Dynamics of Salivary Gland AQP5 under Normal and Pathologic Conditions.International journal of molecular sciences · 2020
    Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Physiological role of aquaporin 5 in salivary glands.Pflugers Archiv : European journal of physiology · 2016
    Review
  20. Aquaporin-5: from structure to function and dysfunction in cancer.Cellular and molecular life sciences : CMLS · 2016
    Review
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

10 authors at 3 institutions in 2 countries.

Chenjuan YaoDepartment of Molecular Oral Physiology, Institute of Health Biosciences, The University of Tokushima Graduate School, Tokushima-shi, Tokushima, Japan.
Nunuk Purwanti
Mileva Ratko Karabasil
Ahmad Azlina
Purevjav Javkhlan
Takahiro Hasegawa
Tetsuya Akamatsu
Toru Hosoi
Koichiro Ozawa
Kazuo Hosoi
Tokushima University · JPBritish Society of Periodontology · GBHiroshima University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The mRNA and protein levels of aquaporin (AQP)5 in the parotid gland were found to be potentially decreased by lipopolysaccharide (LPS) in vivo in C3H/HeN mice, but only weakly in C3H/HeJ, a TLR4 mutant mouse strain. In the LPS-injected mice, pilocarpine-stimulated saliva production was reduced by more than 50%. In a tissue culture system, the LPS-induced decrease in the AQP5 mRNA level was blocked completely by pyrrolidine dithiocarbamate, MG132, tyrphostin AG126, SP600125, and partially by SB203580, which are inhibitors for IkappaB kinase, 26S proteasome, ERK1/2, JNK, and p38 MAPK, respectively. In contrast, the expression of AQP1 mRNA was down-regulated by LPS and such down-regulation was blocked only by SP600125. The transcription factors NF-kappaB (p65 subunit), p-c-Jun, and c-Fos were increased by LPS given in vivo, whereas the protein-binding activities of the parotid gland extract toward the sequences for NF-kappaB but not AP-1-responsive elements present at the promoter region of the AQP5 gene were increased by LPS injection. Co-immunoprecipitation by using antibody columns suggested the physical association of the three transcription factors. These results suggest that LPS-induced potential down-regulation of expression of AQP5 mRNA in the parotid gland is mediated via a complex(es) of these two classes of transcription factors, NF-kappaB and p-c-Jun/c-Fos.

Indexed as

AnimalsAquaporin 1Aquaporin 5Cells, CulturedEnzyme InhibitorsHumansJNK Mitogen-Activated Protein KinasesLipopolysaccharidesMaleMiceMice, Inbred C3HMice, Inbred C57BLNF-kappa BNitratesNitritesProto-Oncogene Proteins c-fosAquaporin 1Aquaporin 5Enzyme InhibitorsJNK Mitogen-Activated Protein KinasesLipopolysaccharidesNF-kappa BNitratesNitritesProto-Oncogene Proteins c-fos

Identifiers

PMID20522648
PMCPMC2913374
OpenAlexW2041820145

What OpenQuestion 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 OpenQuestion graph.