Evidence map›Paper›PMID 22004899›Full record

ArticleJournal of molecular and cellular cardiology2012

β2 adrenergic activation induces the expression of IL-18 binding protein, a potent inhibitor of isoproterenol induced cardiomyocyte hypertrophy in vitro and myocardial hypertrophy in vivo.

David R Murray, Srinivas Mummidi, Anthony J Valente, Tadashi Yoshida, Naveen K Somanna, Patrice Delafontaine, Charles A Dinarello, Bysani Chandrasekar

Open access · greenAbstract read
In one paragraph

Article in Journal of molecular and cellular cardiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

19 citing papers in PubMed, 40 citations in OpenAlex.

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  7. Review
  8. Remifentanil upregulates hepatic IL-18 binding protein (IL-18BP) expression through transcriptional control.Laboratory investigation; a journal of technical methods and pathology · 2018
    Article
  9. Review
  10. Insulin and β Adrenergic Receptor Signaling: Crosstalk in Heart.Trends in endocrinology and metabolism: TEM · 2017
    Review
  11. PDE1C deficiency antagonizes pathological cardiac remodeling and dysfunction.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  12. Article
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  15. Review
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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

8 authors at 4 institutions in 1 country.

David R MurrayWilliam S. Middleton Memorial Veterans Hospital, Madison, WI 53705, United States.
Srinivas Mummidi
Anthony J Valente
Tadashi Yoshida
Naveen K Somanna
Patrice Delafontaine
Charles A Dinarello
Bysani Chandrasekar
Tulane University · USThe University of Texas Health Science Center at San Antonio · USUniversity of Colorado Denver · USWilliam S. Middleton Memorial Veterans Hospital · US

Funding

Insulin-Like Growth Factor-1and AtherosclerosisR01HL070241 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI PATRICE DELAFONTAINE · 2003 to 2026
$10.1M
Yeast-based HTS Assay Technologies for ProteasesR01AI015614 · NIAID · UNIVERSITY OF COLORADO DENVER · PI DINARELLO, CHARLES ANTHONY · 1985 to 2025
$8.5M
CCR5 REGULATION AND PROMOTER VARIANTS IN HIV1 INFECTIONR01AI043279 · NIAID · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI AHUJA, SUNIL K, MUMMIDI, SRINIVAS · 1998 to 2014
$3.6M
ANGIOTENSIN II, IGF-1 AND SKELETAL MUSCLE ATROPHYR01HL080682 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI DELAFONTAINE, PATRICE · 2007 to 2015
$3.3M
The Role of Interleukin-18 in Myocardial Hypertrophy and FailureR01HL086787 · NHLBI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI BYSANI, CHANDRASEKAR · 2009 to 2013
$1.8M
Pathogenesis of Fever in ManR56AI015614 · NIAID · UNIVERSITY OF COLORADO DENVER · PI DINARELLO, CHARLES ANTHONY · 2016 to 2016
$311k
Transcriptional Mechanisms Regulating the HIV-1 coreceptor CCR5I01BX000975 · VA · SOUTH TEXAS VETERANS HEALTH CARE SYSTEM · PI MUMMIDI, SRINIVAS · 2011 to 2015
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PATHOGENESIS OF FEVER IN HUMANSR37AI015614 · NIAID · UNIVERSITY OF COLORADO DENVER · PI DINARELLO, CHARLES ANTHONY · 1988 to 1998
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Interleukin-18 and post infarct myocardial remodelingI01BX000246 · VA · SOUTH TEXAS VETERANS HEALTH CARE SYSTEM · PI BYSANI, CHANDRASEKAR · 2009 to 2013
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BLRD VA I01 BX000246BLRD VA I01 BX000975NHLBI NIH HHS HL-70241NHLBI NIH HHS HL-80682NHLBI NIH HHS HL-86787NHLBI NIH HHS R01 HL070241NHLBI NIH HHS R01 HL080682NHLBI NIH HHS R01 HL086787NIAID NIH HHS AI043279NIAID NIH HHS AI15614NIAID NIH HHS R01 AI015614NIAID NIH HHS R01 AI043279NIAID NIH HHS R56 AI015614
6 · The paper itself

Abstract

Both the sympathetic nervous system and the proinflammatory cytokine interleukin-18 (IL-18) play key roles in the pathophysiology of the hypertrophied failing heart. IL-18 binding protein (IL-18BP), a natural inhibitor of IL-18, counters its biological effects. β-AR stimulation induces IL-18 expression, but whether it also regulates IL-18BP is not known. Here we demonstrate that the β-AR agonist isoproterenol (ISO) increases steady state IL-18BP mRNA and protein levels in adult mouse cardiomyocytes in a β(2)-AR-dependent manner. We cloned mouse Il18bp 5'cis-regulatory region, and identified putative CREB and C/EBPβ transcription factor-binding sites. Forced expression of mutant CREB or C/EBPβ knockdown markedly attenuated ISO-induced Il18bp transcription and deletion or mutation of CREB and C/EBP motifs in the Il18bp promoter reduced ISO-induced promoter-reporter gene activity. ISO induced CREB and C/EBPβ activation in cardiomyocytes via PI3K/Akt and ERK1/2. Importantly, ISO-induced hypertrophy in vitro was dependent on IL-18 induction as it was blunted by IL-18 neutralizing antibodies and forced expression of IL-18BP. Moreover, ISO-induced hypertrophy was markedly attenuated in IL-18 null and IL-18BP transgenic mice. These data support the novel concept that β-AR activation, in addition to inducing cardiomyocyte hypertrophy via IL-18, concomitantly induces a countering effect by stimulating IL-18BP expression, and that ISO-induced cardiomyocyte hypertrophy may result from a net effect of IL-18 and IL-18BP induction.

Indexed as

Adrenergic beta-2 Receptor AgonistsAnimalsCardiomegalyCCAAT-Enhancer-Binding ProteinsCyclic AMP Response Element-Binding ProteinGene Expression RegulationGene Knockout TechniquesIntercellular Signaling Peptides and ProteinsInterleukin-18IsoproterenolMaleMiceMice, Inbred C57BLMice, KnockoutMyocytes, CardiacReceptors, Adrenergic, beta-2Adrenergic beta-2 Receptor AgonistsCCAAT-Enhancer-Binding ProteinsCyclic AMP Response Element-Binding ProteinIntercellular Signaling Peptides and ProteinsInterleukin-18interleukin-18 binding proteinIsoproterenolReceptors, Adrenergic, beta-2

Identifiers

PMID22004899
PMCPMC3246026
OpenAlexW1982570312

What OpenQuestion holds

Textmetadata
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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.