Evidence map›Paper›PMID 16574909›Full record

ArticleCirculation research2006

Scavenger receptor BI prevents nitric oxide-induced cytotoxicity and endotoxin-induced death.

Xiang-An Li, Ling Guo, Reto Asmis, Mariana Nikolova-Karakashian, Eric J Smart

Open access · greenAbstract read
In one paragraph

Article in Circulation research, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
0.3field-weighted citation impact, top 37% 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

24 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Review
  3. The Role of Scavenger Receptor BI in Sepsis.International journal of molecular sciences · 2024
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Scavenger receptor class B type I and immune dysfunctions.Current opinion in endocrinology, diabetes, and obesity · 2014
    Review
  13. HDL and endothelial protection.British journal of pharmacology · 2013
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

5 authors at 1 institution in 1 country.

Xiang-An LiDepartment of Pediatrics, University of Kentucky Medical School, Lexington, KY, USA. xli2@email.uky.edu
Ling Guo
Reto Asmis
Mariana Nikolova-Karakashian
Eric J Smart
University of Kentucky · US

Funding

PROTECTIVE ACTIONS OF ESTRADIOL/SERMS ON BRAIN/HIVP20RR015592 · NCRR · UNIVERSITY OF KENTUCKY · PI KILGORE, MICHAEL · 2000 to 2009
$18.2M
The Interaction of Interleukin 1b and Glucocorticoid Signaling Pathways in Alzheimer's DiseaseR01AG019223 · NIA · UNIVERSITY OF KENTUCKY · PI NIKOLOVA-KARAKASHIAN, MARIANA N · 2002 to 2022
$5.1M
HIV protease inhibitors, marcophage function/estrogenR01HL073693 · NHLBI · UNIVERSITY OF KENTUCKY · PI WILSON, MELINDA E · 2003 to 2007
$1.8M
HIV Protease Inhibitors and AtherosclerosisR01HL068509 · NHLBI · UNIVERSITY OF KENTUCKY · PI SMART, ERIC J · 2002 to 2006
$1.8M
Role of SR-BI in LPS detoxificationR01GM085231 · NIGMS · UNIVERSITY OF KENTUCKY · PI LI, XIANG-AN · 2008 to 2012
$1.5M
Mechanism of Diabetes-associated HypertensionR56DK063025 · NIDDK · UNIVERSITY OF KENTUCKY · PI SMART, ERIC J · 2005 to 2006
$220k
NCRR NIH HHS 2P20RR015592NCRR NIH HHS P20 RR015592NHLBI NIH HHS R01 HL068509NHLBI NIH HHS R01 HL073693NHLBI NIH HHS R01HL073693NHLBI NIH HHS R01HL68509NIA NIH HHS R01 AG019223NIDDK NIH HHS R56 DK063025NIDDK NIH HHS R56DK63025-01A2NIGMS NIH HHS R01 GM085231
6 · The paper itself

Abstract

Nitric oxide (NO)-induced oxidative stress contributes to a variety of diseases. Although numerous mechanisms have been described controlling the production of NO, the mechanisms to prevent NO-induced cytotoxicity after NO synthesis are largely unknown. Here we report that scavenger receptor BI (SR-BI) prevents NO-induced cytotoxicity. Using CHO cell lines expressing wild-type and single-site mutant SR-BI protein, we demonstrate that SR-BI prevents NO-induced cytotoxicity and that a highly conserved CXXS redox motif is required for the anti-NO cytotoxicity activity of SR-BI. Using genetically manipulated mice, we demonstrate that SR-BI-null mice have a 3- to 4-fold increase in tyrosine nitrated proteins in aorta and liver compared with wild-type littermates, indicating that expression of SR-BI prevents peroxynitrite formation in vivo. Using lipopolysacharide (LPS)-challenged mice as an in vivo model of NO-induced cytotoxicity, we found that a single dose of LPS (120,000 U/g IP) induced 90% fatality of SR-BI-null mice within 3 days, whereas all of the wild-type littermates survived (n=20), demonstrating that SR-BI is highly protective against NO cytotoxicity in vivo. Importantly, SR-BI prevents LPS-induced death without eliminating NO production, suggesting that SR-BI prevents NO-induced cytotoxicity post-NO synthesis. Our study describes a novel observation that may shed new light on the treatment of nitric oxidative stress-associated diseases, such as septic shock.

Indexed as

Amino Acid SequenceAnimalsCD36 AntigensCell DeathCHO CellsConserved SequenceCricetinaeEndotoxinsGene DeletionHumansLipopolysaccharidesMiceMice, KnockoutNitric OxideRecombinant ProteinsScavenger Receptors, Class BCD36 AntigensEndotoxinsLipopolysaccharidesNitric OxideRecombinant ProteinsSCARB1 protein, humanScavenger Receptors, Class B

Identifiers

PMID16574909
PMCPMC10961161
OpenAlexW2085333465

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.