Evidence map›Paper›PMID 24447911›Full record

ArticleCellular signalling2014

Docosahexaenoic acid reverses angiotensin II-induced RECK suppression and cardiac fibroblast migration.

Jalahalli M Siddesha, Anthony J Valente, Tadashi Yoshida, Siva S V P Sakamuri, Patrice Delafontaine, Hideo Iba, Makoto Noda, Bysani Chandrasekar

Abstract read
In one paragraph

Article in Cellular signalling, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

21 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
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  3. Expression of Reversion-Inducing Cysteine-Rich Protein with Kazal Motifs (International journal of molecular sciences · 2024
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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 5 institutions in 2 countries.

Jalahalli M SiddeshaResearch Service, Southeast Louisiana Veterans Health Care System, New Orleans, LA 70161, United States; Heart and Vascular Institute, Tulane University School of Medicine, New Orleans, LA 70112, United States.
Anthony J ValenteDepartment of Medicine, University of Texas Health Science Center and South Texas Veterans Health Care System, San Antonio, TX 78229, United States.
Tadashi YoshidaHeart and Vascular Institute, Tulane University School of Medicine, New Orleans, LA 70112, United States.
Siva S V P SakamuriHeart and Vascular Institute, Tulane University School of Medicine, New Orleans, LA 70112, United States.
Patrice DelafontaineHeart and Vascular Institute, Tulane University School of Medicine, New Orleans, LA 70112, United States.
Hideo IbaDepartment of Microbiology and Immunology, University of Tokyo, Tokyo 108-8639, Japan.
Makoto NodaDepartment of Molecular Oncology, Kyoto University Graduate School of Medicine, Sakyo-ku, Kyoto 606-8501, Japan.
Bysani ChandrasekarResearch Service, Southeast Louisiana Veterans Health Care System, New Orleans, LA 70161, United States; Heart and Vascular Institute, Tulane University School of Medicine, New Orleans, LA 70112, United States. Electronic address: bchandra@tulane.edu.
Tulane University · USKyoto University · JPSoutheast Louisiana Veterans Health Care System · USSouth Texas Veterans Health Care System · USThe University of Tokyo · JP

Funding

Insulin-Like Growth Factor-1and AtherosclerosisR01HL070241 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI PATRICE DELAFONTAINE · 2003 to 2026
$10.1M
Translational Research in Hypertension and Renal BiologyP30GM103337 · NIGMS · TULANE UNIVERSITY OF LOUISIANA · PI KOBORI, HIROYUKI · 2012 to 2016
$5.8M
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
Interleukin-18 and post infarct myocardial remodelingI01BX000246 · VA · SOUTH TEXAS VETERANS HEALTH CARE SYSTEM · PI BYSANI, CHANDRASEKAR · 2009 to 2013
–
BLRD VA I01 BX000246NHLBI NIH HHS HL-70241NHLBI NIH HHS HL-80682NHLBI NIH HHS HL-86787NHLBI NIH HHS R01 HL070241NHLBI NIH HHS R01 HL080682NHLBI NIH HHS R01 HL086787NIGMS NIH HHS P30 GM103337
6 · The paper itself

Abstract

The omega-3 polyunsaturated fatty acids (ω-3 fatty acids) eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) have been reported to inhibit or delay the progression of cardiovascular diseases, including myocardial fibrosis. Recently we reported that angiotensin II (Ang II) promotes cardiac fibroblast (CF) migration by suppressing the MMP regulator reversion-inducing-cysteine-rich protein with Kazal motifs (RECK), through a mechanism dependent on AT1, ERK, and Sp1. Here we investigated the role of miR-21 in Ang II-mediated RECK suppression, and determined whether the ω-3 fatty acids reverse these effects. Ang II induced miR-21 expression in primary mouse cardiac fibroblasts (CFs) via ERK-dependent AP-1 and STAT3 activation, and while a miR-21 inhibitor reversed Ang II-induced RECK suppression, a miR-21 mimic inhibited both RECK expression and Ang II-induced CF migration. Moreover, Ang II suppressed the pro-apoptotic PTEN, and the ERK negative regulator Sprouty homologue 1 (SPRY1), but induced the metalloendopeptidase MMP2, all in a manner that was miR-21-dependent. Further, forced expression of PTEN inhibited Akt phosphorylation, Sp1 activation, and MMP2 induction. Notably, while both EPA and DHA reversed Ang II-mediated RECK suppression, DHA appeared to be more effective, and reversed Ang II-induced miR-21 expression, RECK suppression, MMP2 induction, and CF migration. These results indicate that Ang II-induced CF migration is differentially regulated by miR-21-mediated MMP induction and RECK suppression, and that DHA has the potential to upregulate RECK, and therefore may exert potential beneficial effects in cardiac fibrosis.

Indexed as

3' Untranslated RegionsAdaptor Proteins, Signal TransducingAngiotensin IIAnimalsCell MovementCells, CulturedDocosahexaenoic AcidsExtracellular Signal-Regulated MAP KinasesFibroblastsGPI-Linked ProteinsMaleMatrix Metalloproteinase 2Membrane ProteinsMiceMice, Inbred C57BLMicroRNAs3' Untranslated RegionsAdaptor Proteins, Signal TransducingAngiotensin IIDocosahexaenoic AcidsExtracellular Signal-Regulated MAP KinasesGPI-Linked ProteinsMatrix Metalloproteinase 2Membrane ProteinsMicroRNAsMIRN21 microRNA, mousePhosphoproteinsPTEN PhosphohydrolasePten protein, mouseReck protein, mouseSpry1 protein, mouseStat3 protein, mouseSTAT3 Transcription FactorTranscription Factor AP-1FibrosisMicroRNAPTENRECKSPRY1ω−3 lipids

Identifiers

PMID24447911
PMCPMC3951845
OpenAlexW1980771525

What OpenQuestion holds

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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.