Evidence map›Paper›PMID 26692198›Full record

ArticlePloS one2015

Endothelial Cell Surface Expressed Chemotaxis and Apoptosis Regulator (ECSCR) Regulates Lipolysis in White Adipocytes via the PTEN/AKT Signaling Pathway.

Sreenivasulu Kilari, Stephanie Cossette, Shabnam Pooya, Michelle Bordas, Yi-Wen Huang, Ramani Ramchandran, George A Wilkinson

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.6field-weighted citation impact, top 28% 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

3 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
  2. The Role of MicroRNA-21 in Venous Neointimal Hyperplasia: Implications for Targeting miR-21 for VNH Treatment.Molecular therapy : the journal of the American Society of Gene Therapy · 2019
    Article
  3. A role for miR-132 in learned safety.Scientific reports · 2019
    Article
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 1 country.

Sreenivasulu KilariDepartment of Pediatrics and Developmental Vascular Biology Program, Medical College of Wisconsin and Children's Research Institute, Milwaukee, Wisconsin, United States of America.
Stephanie CossetteDepartment of Pediatrics and Developmental Vascular Biology Program, Medical College of Wisconsin and Children's Research Institute, Milwaukee, Wisconsin, United States of America.
Shabnam PooyaDepartment of Pediatrics and Developmental Vascular Biology Program, Medical College of Wisconsin and Children's Research Institute, Milwaukee, Wisconsin, United States of America.
Michelle BordasDepartment of Pediatrics and Developmental Vascular Biology Program, Medical College of Wisconsin and Children's Research Institute, Milwaukee, Wisconsin, United States of America.
Yi-Wen HuangDepartment of Obstetrics and Gynecology, Medical College of Wisconsin and Children's Research Institute, Milwaukee, Wisconsin, United States of America.
Ramani RamchandranDepartment of Pediatrics and Developmental Vascular Biology Program, Medical College of Wisconsin and Children's Research Institute, Milwaukee, Wisconsin, United States of America.
George A WilkinsonDepartment of Pediatrics and Developmental Vascular Biology Program, Medical College of Wisconsin and Children's Research Institute, Milwaukee, Wisconsin, United States of America.
Medical College of Wisconsin · USChildren's Hospital of Wisconsin · US

Funding

Targeting DUSP-5 to Treat Vascular AnomaliesR01HL112639 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI RAMCHANDRAN, RAMANI · 2012 to 2016
$2.6M
Snrk-1 and Dusp-5 co-ordinately regulate vascular development in vertebratesR01HL102745 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI RAMCHANDRAN, RAMANI · 2011 to 2014
$1.5M
NHLBI NIH HHS 1R01 HL09712NHLBI NIH HHS 1R01HL102745-01NHLBI NIH HHS 1R01HL112639-01NHLBI NIH HHS R01 HL102745NHLBI NIH HHS R01 HL112639
6 · The paper itself

Abstract

Elevated plasma triglycerides are associated with increased susceptibility to heart disease and stroke, but the mechanisms behind this relationship are unclear. A clearer understanding of gene products which influence plasma triglycerides might help identify new therapeutic targets for these diseases. The Endothelial Cell Surface expressed Chemotaxis and apoptosis Regulator (ECSCR) was initially studied as an endothelial cell marker, but has recently been identified in white adipocytes, the primary storage cell type for triglycerides. Here we confirm ECSCR expression in white adipocytes and show that Ecscr knockout mice show elevated fasting plasma triglycerides. At a cellular level, cultured 3T3-L1 adipocytes silenced for Ecscr show a blunted Akt phosphorylation response. Additionally we show that the phosphatase and tensin homology containing (PTEN) lipid phosphatase association with ECSCR is increased by insulin stimulation. These data suggest a scenario by which ECSCR contributes to control of white adipocyte lipolysis. In this scenario, white adipocytes lacking Ecscr display elevated PTEN activity, thereby reducing AKT activation and impairing insulin-mediated suppression of lipolysis. Collectively, these results suggest that ECSCR plays a critical function in regulating lipolysis in white adipose tissue.

Indexed as

3T3-L1 CellsAdipocytes, WhiteAnimalsApoptosis Regulatory ProteinsLipolysisMembrane ProteinsMiceMice, KnockoutProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseSignal TransductionTriglyceridesApoptosis Regulatory ProteinsEcscr protein, mouseMembrane ProteinsProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, humanTriglycerides

Identifiers

PMID26692198
PMCPMC4686900
OpenAlexW2202656845

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.