Evidence map›Paper›PMID 22523073›Full record

ArticleThe Journal of biological chemistry2012

Toll-like receptor 2 is required for LPS-induced Toll-like receptor 4 signaling and inhibition of ion transport in renal thick ascending limb.

David W Good, Thampi George, Bruns A Watts

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
2.9field-weighted citation impact, top 10% 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

41 citing papers in PubMed, 69 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. The Controversial Role of LPS in Platelet Activation In Vitro.International journal of molecular sciences · 2022
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Toll-Like Receptor as a Potential Biomarker in Renal Diseases.International journal of molecular sciences · 2020
    Review
  15. Article
  16. Article
  17. Article
  18. 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

3 authors at 1 institution in 1 country.

David W GoodDepartments of Internal Medicine, University of Texas Medical Branch, Galveston, Texas 77555, USA. dgood@utmb.edu
Thampi George
Bruns A Watts
The University of Texas Medical Branch at Galveston · US

Funding

REGULATION OF THICK ASCENDING LIMB ACID-BASE TRANSPORTR01DK038217 · NIDDK · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI GOOD, DAVID WILLIAM · 1987 to 2019
$5.0M
NIDDK NIH HHS DK-038217NIDDK NIH HHS R01 DK038217
6 · The paper itself

Abstract

Previously we demonstrated that basolateral LPS inhibits HCO(3)(-) absorption in the renal medullary thick ascending limb (MTAL) through TLR4-dependent ERK activation. Here we report that the response of the MTAL to basolateral LPS requires TLR2 in addition to TLR4. The basolateral addition of LPS (ultrapure Escherichia coli K12) decreased HCO(3)(-) absorption in isolated, perfused MTALs from wild-type mice but had no effect in MTALs from TLR2(-/-) mice. In contrast, inhibition of HCO(3)(-) absorption by lumen LPS was preserved in TLR2(-/-) MTALs, indicating that TLR2 is involved specifically in mediating the basolateral LPS response. LPS also did not increase ERK phosphorylation in MTALs from TLR2(-/-) mice. TLR2 deficiency had no effect on expression of TLR4, MD-2, or MyD88. However, LPS-induced recruitment of MyD88 to the basolateral membrane was impaired in TLR2(-/-) MTALs. Inhibition of HCO(3)(-) absorption by LPS did not require CD14. Co-immunoprecipitation studies demonstrated an association between TLR4 and TLR2. Inhibition of HCO(3)(-) absorption by TLR2-specific ligands was preserved in MTALs from TLR4(-/-) mice. These results indicate that the effect of basolateral LPS to inhibit HCO(3)(-) absorption in the MTAL through MyD88-dependent ERK activation depends on a novel interaction between TLR4 and TLR2. TLR2 plays a dual role in the induction of intracellular signals that impair MTAL function, both through cooperation with TLR4 to mediate ERK signaling by LPS and through a TLR4-independent signaling pathway activated by Gram-positive bacterial ligands. Regulation of TLR2 expression and its interaction with TLR4 may provide new mechanisms for controlling and therapeutic targeting of TLR4-mediated LPS responses.

Indexed as

AnimalsCarbonatesExtracellular Signal-Regulated MAP KinasesGene Expression RegulationIon TransportKidney MedullaLipopolysaccharide ReceptorsLipopolysaccharidesMaleMAP Kinase Signaling SystemMiceMice, KnockoutMyeloid Differentiation Factor 88PhosphorylationRatsRats, Sprague-DawleyCarbonatesExtracellular Signal-Regulated MAP KinasesLipopolysaccharide ReceptorsLipopolysaccharidesMyd88 protein, mouseMyd88 protein, ratMyeloid Differentiation Factor 88Tlr2 protein, mouseTlr2 protein, ratTlr4 protein, mouseTlr4 protein, ratToll-Like Receptor 2Toll-Like Receptor 4

Identifiers

PMID22523073
PMCPMC3370203
OpenAlexW1979413396

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.