Evidence map›Paper›PMID 24918749›Full record

ArticleMolecular medicine (Cambridge, Mass.)2014

Human myocardium releases heat shock protein 27 (HSP27) after global ischemia: the proinflammatory effect of extracellular HSP27 through toll-like receptor (TLR)-2 and TLR4.

Chunhua Jin, Joseph C Cleveland, Lihua Ao, Jilin Li, Qingchun Zeng, David A Fullerton, Xianzhong Meng

Open access · goldAbstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed
5.0field-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

77 citing papers in PubMed, 122 citations in OpenAlex.

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

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

7 authors at 2 institutions in 2 countries.

Chunhua JinDepartment of Surgery, University of Colorado Denver, Aurora, Colorado, United States of America Center for Experimental Medicine, Southern Medical University, Guangzhou, China.
Joseph C ClevelandDepartment of Surgery, University of Colorado Denver, Aurora, Colorado, United States of America.
Lihua AoDepartment of Surgery, University of Colorado Denver, Aurora, Colorado, United States of America.
Jilin LiDepartment of Surgery, University of Colorado Denver, Aurora, Colorado, United States of America Department of Cardiology, Southern Medical University, Guangzhou, China.
Qingchun ZengDepartment of Surgery, University of Colorado Denver, Aurora, Colorado, United States of America Department of Cardiology, Southern Medical University, Guangzhou, China.
David A FullertonDepartment of Surgery, University of Colorado Denver, Aurora, Colorado, United States of America.
Xianzhong MengDepartment of Surgery, University of Colorado Denver, Aurora, Colorado, United States of America.
University of Colorado Denver · USSouthern Medical University · CN

Funding

Inflammatory response of aging heart to surgical myocardial ischemiaR01AG039545 · NIA · UNIVERSITY OF COLORADO DENVER · PI MENG, XIANZHONG · 2011 to 2015
$1.5M
NIA NIH HHS AG039545NIA NIH HHS R01 AG039545
6 · The paper itself

Abstract

The myocardial inflammatory response contributes to cardiac functional injury associated with heart surgery obligating global ischemia/reperfusion (I/R). Toll-like receptors (TLRs) play an important role in the mechanism underlying myocardial I/R injury. The aim of this study was to examine the release of small constitutive heat shock proteins (HSPs) from human and mouse myocardium after global ischemia and examine the role of extracellular small HSP in myocardial injury. HSP27 release was assessed by enzyme-linked immunosorbent assay. Anti-HSP27 was applied to evaluate the role of extracellular HSP27 in the postischemic inflammatory response and functional injury in mouse hearts. Isolated hearts and cultured coronary vascular endothelial cells were exposed to recombinant HSP27 to determine its effect on proinflammatory signaling and production of proinflammatory mediators. HSP27 levels were markedly elevated in coronary sinus blood of patients and in coronary effluent of mouse hearts after global ischemia. Neutralizing extracellular HSP27 suppressed myocardial nuclear factor (NF)-κB activation and interleukin (IL)-6 production and improved cardiac function in mouse hearts. Perfusion of HSP27 to mouse hearts induced NF-κB activation and IL-6 production and depressed contractility. Further, recombinant HSP27 induced NF-κB phosphorylation and upregulated monocyte chemoattractant protein (MCP)-1 and intercellular adhesion molecule (ICAM)-1 production in both human and mouse coronary vascular endothelial cells. TLR2 knockout (KO) or TLR4 mutation abolished NF-κB phosphorylation and reduced MCP-1 and ICAM-1 production induced by extracellular HSP27 in endothelial cells. In conclusion, these results show that the myocardium releases HSP27 after global ischemia and that extracellular HSP27 is proinflammatory and contributes to the inflammatory mechanism of myocardial functional injury. Both TLR2 and TLR4 are involved in mediating the proinflammatory effect of extracellular HSP27.

Indexed as

AnimalsCells, CulturedCytokinesEndothelial CellsHeat-Shock ProteinsHSP27 Heat-Shock ProteinsHumansIntercellular Adhesion Molecule-1MaleMice, Inbred C3HMice, Inbred C57BLMice, KnockoutMolecular ChaperonesMyocardial Reperfusion InjuryMyocardiumNF-kappa BCytokinesHeat-Shock ProteinsHSP27 Heat-Shock ProteinsHSPB1 protein, humanHspb2 protein, mouseIntercellular Adhesion Molecule-1Molecular ChaperonesNF-kappa BTLR2 protein, humanTlr2 protein, mouseTLR4 protein, humanTlr4 protein, mouseToll-Like Receptor 2Toll-Like Receptor 4

Identifiers

PMID24918749
PMCPMC4107099
OpenAlexW2129824195

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.