Evidence map›Paper›PMID 15793305›Full record

ArticleThe American journal of pathology2005

Macrophage conditioned medium induces the expression of C-reactive protein in human aortic endothelial cells: potential for paracrine/autocrine effects.

Senthil Kumar Venugopal, Sridevi Devaraj, Ishwarlal Jialal

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
10.3field-weighted citation impact, top 1% 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

56 citing papers in PubMed, 155 citations in OpenAlex.

  1. Trial
  2. Biomarkers of Cardiovascular Stress: A Historical Review.Journal of cardiovascular development and disease · 2026
    Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. C-Reactive Protein, Uric Acid, and Coronary Artery Ectasia in Patients with Coronary Artery Disease.Medical science monitor : international medical journal of experimental and clinical research · 2025
    Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. The secretome mouse provides a genetic platform to delineate tissue-specific in vivo secretion.Proceedings of the National Academy of Sciences of the United States of America · 2021
    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.

Senthil Kumar VenugopalLaboratory for Atherosclerosis and Metabolic Research, Department of Pathology and Laboratory Medicine, University of California Medical Center, Sacramento, CA 95817, USA.
Sridevi Devaraj
Ishwarlal Jialal
University of California Davis Medical Center · US

Funding

Using Technology to Enhance Cancer Communication and Improve Clinical OutcomesP50CA095817 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI BAKER, TIMOTHY B · 2003 to 2012
$19.3M
CRP, Diabetes, AtherothrombosisR01HL074360 · NHLBI · UNIVERSITY OF CALIFORNIA DAVIS · PI JIALAL, ISHWARLAL · 2004 to 2010
$2.3M
CLINICAL STUDIES IN NUTRITION AND METABOLISMK24AT000596 · NCCIH · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI JIALAL, ISHWARLAL · 2000 to 2009
$1.3M
NCCIH NIH HHS K24 AT000596NCCIH NIH HHS K24AT00596NCI NIH HHS P50 CA095817NHLBI NIH HHS R01 HL074360
6 · The paper itself

Abstract

C-reactive protein (CRP) is a risk marker for cardiovascular events in apparently healthy persons. Cogent data show that, aside from the liver, CRP is produced in atherosclerotic lesions, kidney, neurons, and alveolar macrophages. Because several proatherogenic effects of CRP have been documented in endothelial cells, we examined human aortic endothelial cells (HAEC) for CRP production. We detected the presence of CRP mRNA by RT-PCR and in situ hybridization, intracellular protein by Western blot and secreted protein by ELISA. Coincubation with the cytokines interleukin (IL)-1, IL-6, and tumor necrosis factor alone and in combination showed that the most potent agonist for CRP production from HAEC is the combination of IL-1 and IL-6 (P < 0.05). To mimic the in vivo situation, we examined whether vascular smooth muscle cell (VSMC) and/or macrophage conditioned media (MCM) could augment CRP production by HAEC. While VSMC-conditioned media had no effect, incubation with MCM resulted in a significant twofold increase in the synthesis of both intracellular and secreted CRP (P < 0.05). The effect of MCM could be reversed by inhibiting both IL-1 and IL-6. Thus, stimulated synthesis and secretion of CRP by cells in the atherosclerotic lesion by paracrine/autocrine loops could result in local concentrations of CRP far in excess of plasma concentrations and could contribute to proinflammatory, proatherogenic effects.

Indexed as

Autocrine CommunicationParacrine CommunicationAortaBlotting, WesternCells, CulturedCoronary VesselsC-Reactive ProteinCulture Media, ConditionedCytokinesEndothelial CellsEnzyme-Linked Immunosorbent AssayHumansIn Situ HybridizationMacrophagesRNA, MessengerUmbilical VeinsC-Reactive ProteinCulture Media, ConditionedCytokinesRNA, Messenger

Identifiers

PMID15793305
PMCPMC1602373
OpenAlexW1599229285

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.