Evidence map›Paper›PMID 19417089›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2009

HDL antielastase activity prevents smooth muscle cell anoikis, a potential new antiatherogenic property.

Guadalupe Ortiz-Muñoz, Xavier Houard, Jose-Luis Martín-Ventura, Brian Y Ishida, Stéphane Loyau, Patrick Rossignol, Juan-Antonio Moreno, John P Kane, Robert J Chalkley, Alma L Burlingame and 2 more

Open access · greenAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
2.6field-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

49 citing papers in PubMed, 1 synthesis or guideline pooled it, 97 citations in OpenAlex.

  1. Pooled it
  2. High-density lipoproteins limit neutrophil-induced damage to the blood-brain barrier in vitro.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2013
    Trial
  3. Review
  4. Review
  5. Article
  6. ANGPTL3 is a novel HDL component that regulates HDL function.Journal of translational medicine · 2024
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. The HDL Proteome Watch: Compilation of studies leads to new insights on HDL function.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2022
    Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Post-Translational Modifications of Circulating Alpha-1-Antitrypsin Protein.International journal of molecular sciences · 2020
    Review
  19. Review
  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

12 authors at 4 institutions in 2 countries.

Guadalupe Ortiz-MuñozINSERM U698, Paris, France.
Xavier Houard
Jose-Luis Martín-Ventura
Brian Y Ishida
Stéphane Loyau
Patrick Rossignol
Juan-Antonio Moreno
John P Kane
Robert J Chalkley
Alma L Burlingame
Jean-Baptiste Michel
Olivier Meilhac
Inserm · FRUniversity of California, San Francisco · USUniversité Paris Cité · FRHôpital Jeanne d'Arc · FR

Funding

YEAST THREONINE &SERINE KINASESP41RR001614 · NCRR · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ORTIZ DE MONTELLANO, PAUL R · 1985 to 2011
$24.1M
NCRR NIH HHS P41 RR001614NCRR NIH HHS RR01614
6 · The paper itself

Abstract

Various studies using proteomic approaches have shown that HDL can carry many proteins other than its constitutive apolipoprotein A-I (apoA-I). Using mass spectrometry and Western blotting, we showed the presence of alpha(1)-antitrypsin (AAT) (SERPINA1, serpin peptidase inhibitor, clade A, an elastase inhibitor) in HDL, isolated either by ultracentrifugation or by selected-affinity immunosorption using an anti-apoA-I column. Furthermore, we report that HDL possesses potent antielastase activity. We further showed that only HDL but not LDL is able to bind AAT. HDL-associated AAT was able to inhibit extracellular matrix degradation, cell detachment, and apoptosis induced by elastase in human vascular smooth muscle cells (VSMCs) and in mammary artery cultured ex vivo. Degradation of fibronectin by elastase used as a marker of pericellular proteolysis was prevented by addition of HDL. Elastase present in aortic abdominal aneurysm (AAA) thrombus samples was also able to induce apoptosis of VSMCs in culture. This phenomenon was prevented by addition of HDL but not of LDL. Finally, we report that the proportion of AAT in HDL isolated from patients with an AAA is decreased relative to that from matched control subjects, suggesting a reduced capacity of HDL to inhibit elastase in these patients. In conclusion, our data provide evidence of a new potential antiatherogenic property of HDL attributable to AAT and its antielastase activity.

Indexed as

Anoikisalpha 1-AntitrypsinAtherosclerosisHumansLipoproteins, HDLMuscle, Smooth, VascularMyocytes, Smooth MusclePancreatic ElastaseProtein BindingProteinsalpha 1-AntitrypsinLipoproteins, HDLPancreatic ElastaseProteins

Identifiers

PMID19417089
PMCPMC2735359
OpenAlexW1989463629

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.