Evidence map›Paper›PMID 22589557›Full record

ArticleJournal of lipid research2012

Macrophage SR-BI regulates LPS-induced pro-inflammatory signaling in mice and isolated macrophages.

Lei Cai, Zhen Wang, Jason M Meyer, Ailing Ji, Deneys R van der Westhuyzen

Open access · hybridAbstract read
In one paragraph

Article in Journal of lipid research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

39 citing papers in PubMed, 68 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. The Role of Scavenger Receptor BI in Sepsis.International journal of molecular sciences · 2024
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. HDL and Scavenger Receptor Class B Type I (SRBI).Advances in experimental medicine and biology · 2022
    Review
  15. Article
  16. Article
  17. Scavenger Receptor BI Attenuates IL-17A-Dependent Neutrophilic Inflammation in Asthma.American journal of respiratory cell and molecular biology · 2021
    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

5 authors at 2 institutions in 2 countries.

Lei CaiDepartment of Veterans Affairs Medical Center, Lexington, KY, USA.
Zhen Wang
Jason M Meyer
Ailing Ji
Deneys R van der Westhuyzen
University of Kentucky · USLexington VA Health Care System · US

Funding

Mouse CoreP01HL086670 · NHLBI · UNIVERSITY OF KENTUCKY · PI VAN DER WESTHUYZEN, DENEYS REM · 2007 to 2011
$7.1M
Class B Scavenger Receptors and AtherosclerosisI01BX000672 · VA · VA MEDICAL CENTER - LEXINGTON, KY · PI VAN DER WESTHUYZEN, DENEYS REM · 2009 to 2013
–
BLRD VA I01 BX000672NHLBI NIH HHS P01 HL086670NHLBI NIH HHS P01-HL-086670-04
6 · The paper itself

Abstract

Scavenger receptor BI (SR-BI), an HDL receptor, plays a key role in reverse cholesterol transport. In mice, disruption of SR-BI results in hypersensitivity to lipopolysaccharide (LPS) and bacteria-induced septic shock due to adrenal insufficiency and abnormal hepatic pathogen clearance. In this study, we identify an anti-inflammatory role of macrophage SR-BI. Using bone marrow transplantation, we report an enhanced pro-inflammatory response to LPS in wild-type (WT) mice receiving SR-BI-null compared with WT bone marrow cells and a reduced response in SR-BI-null mice receiving WT compared with SR-BI-null cells. Although significant, SR-BI deficiency limited to bone marrow-derived cells promoted a relatively modest enhancement of the inflammatory response to LPS in mice compared with the effect of whole-body SR-BI deletion. Consistent with earlier findings, SR-BI-null primary macrophages exhibited a greater inflammatory cytokine response to LPS than control macro phages. In addition, we showed that overexpression of SR-BI in J774 macrophages attenuated the inflammatory response to LPS. The LPS-induced cytokine expression in both WT and SR-BI-null macrophages was dependent not only on NFκB as previously reported but also on JNK and P38 cell signaling pathways. The increased inflammatory signaling in SR-BI-null cells was not related to alterations in cellular cholesterol content. We conclude that SR-BI plays an important function in regulating the macrophage inflammatory response to LPS.

Indexed as

AnimalsBiological TransportBone Marrow TransplantationCD36 AntigensCell SeparationCholesterolCytokinesGene DeletionGene Expression RegulationInflammationJNK Mitogen-Activated Protein KinasesLipopolysaccharidesMacrophagesMaleMiceNF-kappa BCD36 AntigensCholesterolCytokinesJNK Mitogen-Activated Protein KinasesLipopolysaccharidesNF-kappa Bp38 Mitogen-Activated Protein Kinases

Identifiers

PMID22589557
PMCPMC3540840
OpenAlexW2018767491

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.