Evidence map›Paper›PMID 16574901›Full record

ArticleCirculation research2006

Monocyte chemoattractant protein-1 induces a novel transcription factor that causes cardiac myocyte apoptosis and ventricular dysfunction.

Limei Zhou, Asim Azfer, Jianli Niu, Sarabeth Graham, Mahua Choudhury, Frances M Adamski, Craig Younce, Phillip F Binkley, Pappachan E Kolattukudy

Open access · bronzeAbstract 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 142 papers.

0numbers the graph read from it
0cells of the map it votes in
142citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

142 citing papers in PubMed, 256 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
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  6. Review
  7. Macrophage Zc3h12c Limits Tissue Inflammation and Injury via Alternative Splicing of Pre-mRNA.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  8. Review
  9. The Role of MCPIP1 in Macrophage Polarization and Cardiac Function Post-Myocardial Infarction.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Inhibition of visceral adipose tissue-derived pathogenic signals by activation of adenosine AAmerican journal of physiology. Gastrointestinal and liver physiology · 2024
    Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

82 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 1 institution in 1 country.

Limei ZhouBurnett College of Biomedical Sciences, University of Central Florida, Orlando, FL 32816-2364, USA.
Asim Azfer
Jianli Niu
Sarabeth Graham
Mahua Choudhury
Frances M Adamski
Craig Younce
Phillip F Binkley
Pappachan E Kolattukudy
University of Central Florida · US

Funding

MCP-1 induced gene expression in cardiovascular diseaseR01HL069458 · NHLBI · UNIVERSITY OF CENTRAL FLORIDA · PI KOLATTUKUDY, PAPPACHAN · 2002 to 2005
$1.4M
PARADIGM SHIFTS IN CLINICAL ISCHEMIA DETECTIONK24HL004208 · NHLBI · OHIO STATE UNIVERSITY · PI BINKLEY, PHILIP F · 2000 to 2002
$362k
MCPIP, a novel transcription factor in the development of heart failureR56HL069458 · NHLBI · UNIVERSITY OF CENTRAL FLORIDA · PI KOLATTUKUDY, PAPPACHAN KOLATTUKUDY · 2009 to 2009
$355k
NHLBI NIH HHS HL 69458NHLBI NIH HHS K24 HL004208NHLBI NIH HHS K24-HL04208NHLBI NIH HHS R01 HL069458
6 · The paper itself

Abstract

Monocyte chemoattractant protein-1 (MCP-1; CCL2)-mediated inflammation plays a critical role in the development of ischemic heart disease (IHD). However, the gene expression changes caused by signal transduction, triggered by MCP-1 binding to its receptor CCR2, and their possible role in the development of IHD are not understood. We present evidence that MCP-1 binding to CCR2 induces a novel transcription factor (MCP-induced protein [MCPIP]) that causes cell death. Gene microarray analysis showed that when expressed in hiuman embryonic kidney 293 cells, MCPIP induced apoptotic gene families before causing cell death. Mutagenesis studies showed that the structural features required for transcription factor-like activity were also required for causing cell death. Activation of caspase-3 was detected after MCPIP transfection and Z-VAD-fmk partially inhibited cell death. Cardiomyocyte-targeted expression of MCP-1 in mice caused death by heart failure at 6 months of age. MCPIP expression increased in parallel with the development of ventricular dysfunction. In situ hybridization showed the presence of MCPIP transcripts in the cardiomyocytes and immunohistochemistry showed that MCPIP was associated with the cardiomyocyte nuclei of apoptotic cardiomyocytes. CCR2 expression in cardiomyocytes increased with the development of IHD. MCPIP production induced by MCP-1 binding to CCR2 in the cardiomyocytes is probably involved in the development of IHD in this murine model. MCPIP transcript levels were much higher in the explanted human hearts with IHD than with nonischemic heart disease. These results provide a molecular insight into how chronic inflammation and exposure to MCP-1 contributes to heart failure and suggest that MCPIP could be a potential target for therapeutic intervention.

Indexed as

ApoptosisAnimalsCell DeathCell NucleusCells, CulturedChemokine CCL2HumansMiceMice, TransgenicMolecular Sequence DataMyocardial IschemiaMyocardiumMyocytes, CardiacOligonucleotide Array Sequence AnalysisReceptors, CCR2Receptors, ChemokineCCR2 protein, humanCcr2 protein, mouseChemokine CCL2Receptors, CCR2Receptors, ChemokineRibonucleasesTranscription FactorsZC3H12A protein, human

Identifiers

PMID16574901
PMCPMC1523425
OpenAlexW2165984084

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.