Evidence map›Paper›PMID 28982073›Full record

ArticleRedox biology2018

Cardiac-specific inactivation of LPP3 in mice leads to myocardial dysfunction and heart failure.

Mini Chandra, Diana Escalante-Alcalde, Md Shenuarin Bhuiyan, Anthony Wayne Orr, Christopher Kevil, Andrew J Morris, Hyung Nam, Paari Dominic, Kevin J McCarthy, Sumitra Miriyala and 1 more

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
5.5field-weighted citation impact, top 3% 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

44 citing papers in PubMed, 71 citations in OpenAlex.

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  19. Autotaxin-LPA-LPP3 Axis in Energy Metabolism and Metabolic Disease.International journal of molecular sciences · 2021
    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

11 authors at 3 institutions in 2 countries.

Mini ChandraDepartment of Cellular Biology and Anatomy, Louisiana State University Health Sciences Center, Shreveport, USA.
Diana Escalante-AlcaldeDivisión de Neurociencias, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, México DF, Mexico.
Md Shenuarin BhuiyanDepartment of Pathology and Translational Pathobiology, Louisiana State University Health Sciences Center, Shreveport, USA.
Anthony Wayne OrrDepartment of Pathology and Translational Pathobiology, Louisiana State University Health Sciences Center, Shreveport, USA.
Christopher KevilDepartment of Pathology and Translational Pathobiology, Louisiana State University Health Sciences Center, Shreveport, USA.
Andrew J MorrisDivision of Cardiovascular Medicine, University of Kentucky, Lexington, USA.
Hyung NamDepartment of Pharmacology and Toxicology, Louisiana State University Health Sciences Center, Shreveport, USA.
Paari DominicDivision of Cardiology, Department of Medicine, Louisiana State University Health Sciences Center, Shreveport, USA.
Kevin J McCarthyDepartment of Cellular Biology and Anatomy, Louisiana State University Health Sciences Center, Shreveport, USA; Department of Pathology and Translational Pathobiology, Louisiana State University Health Sciences Center, Shreveport, USA.
Sumitra MiriyalaDepartment of Cellular Biology and Anatomy, Louisiana State University Health Sciences Center, Shreveport, USA. Electronic address: smiriy@lsuhsc.edu.
Manikandan PanchatcharamDepartment of Cellular Biology and Anatomy, Louisiana State University Health Sciences Center, Shreveport, USA. Electronic address: mpanch@lsuhsc.edu.
Louisiana State University Health Sciences Center Shreveport · USUniversidad Nacional Autónoma de México · MXUniversity of Kentucky · US

Funding

Nck Adaptor Proteins in Atherogenic Endothelial ActivationR01HL133497 · NHLBI · LOUISIANA STATE UNIV HSC SHREVEPORT · PI ORR, ANTHONY WAYNE · 2016 to 2024
$3.8M
Matrix Signaling in Endothelial Cell DysfunctionR01HL098435 · NHLBI · LOUISIANA STATE UNIV HSC SHREVEPORT · PI ORR, ANTHONY WAYNE · 2010 to 2020
$3.2M
Sigma-1 receptor and cardioprotectionR00HL122354 · NHLBI · LOUISIANA STATE UNIV HSC SHREVEPORT · PI BHUIYAN, MD. SHENUARIN · 2015 to 2017
$747k
Alcohol-LPP3 axis in ischemic strokeR21AA025744 · NIAAA · LOUISIANA STATE UNIV HSC SHREVEPORT · PI PANCHATCHARAM, MANIKANDAN · 2017 to 2018
$483k
Lysophosphatidic acid and cardiovascular disease riskI01CX001550 · VA · VA MEDICAL CENTER - LEXINGTON, KY · PI MORRIS, ANDREW J · 2017 to 2021
–
CSRD VA I01 CX001550NHLBI NIH HHS R00 HL122354NHLBI NIH HHS R01 HL098435NHLBI NIH HHS R01 HL133497NIAAA NIH HHS R21 AA025744
6 · The paper itself

Abstract

Lipid Phosphate phosphatase 3 (LPP3), encoded by the Plpp3 gene, is an enzyme that dephosphorylates the bioactive lipid mediator lysophosphatidic acid (LPA). To study the role of LPP3 in the myocardium, we generated a cardiac specific Plpp3 deficient mouse strain. Although these mice were viable at birth in contrast to global Plpp3 knockout mice, they showed increased mortality ~ 8 months. LPP3 deficient mice had enlarged hearts with reduced left ventricular performance as seen by echocardiography. Cardiac specific Plpp3 deficient mice had longer ventricular effective refractory periods compared to their Plpp3 littermates. We observed that lack of Lpp3 enhanced cardiomyocyte hypertrophy based on analysis of cell surface area. We found that lack of Lpp3 signaling was mediated through the activation of Rho and phospho-ERK pathways. There are increased levels of fetal genes Natriuretic Peptide A and B (Nppa and Nppb) expression indicating myocardial dysfunction. These mice also demonstrate mitochondrial dysfunction as evidenced by a significant decrease (P < 0.001) in the basal oxygen consumption rate, mitochondrial ATP production, and spare respiratory capacity as measured through mitochondrial bioenergetics. Histology and transmission electron microscopy of these hearts showed disrupted sarcomere organization and intercalated disc, with a prominent disruption of the cristae and vacuole formation in the mitochondria. Our findings suggest that LPA/LPP3-signaling nexus plays an important role in normal function of cardiomyocytes.

Indexed as

AnimalsEnergy MetabolismGene DeletionHeart FailureLysophospholipidsMaleMAP Kinase Signaling SystemMiceMice, Inbred C57BLMice, KnockoutMitochondria, HeartMyocardiumOxygen ConsumptionPhosphatidate PhosphataseSignal Transductionlysophosphatidic acidLysophospholipidsPhosphatidate PhosphatasePlpp3 protein, mouseHeart failureLipid phosphate phosphataseLysophosphatidic acid

Identifiers

PMID28982073
PMCPMC5635346
OpenAlexW2757954031

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.