Evidence map›Paper›PMID 28710369›Full record

ArticleScientific reports2017

The adipokine leptin modulates adventitial pericyte functions by autocrine and paracrine signalling.

Federica Riu, Sadie C Slater, Eva Jover Garcia, Iker Rodriguez-Arabaolaza, Valeria Alvino, Elisa Avolio, Giuseppe Mangialardi, Andrea Cordaro, Simon Satchell, Carlo Zebele and 3 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

7 citing papers in PubMed, 15 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 3 institutions in 1 country.

Federica RiuBristol Heart Institute, School of Clinical Sciences, University of Bristol, Bristol Royal Infirmary, Bristol, BS2 8HW, United Kingdom.
Sadie C SlaterBristol Heart Institute, School of Clinical Sciences, University of Bristol, Bristol Royal Infirmary, Bristol, BS2 8HW, United Kingdom.ORCID 0000-0003-3485-3207
Eva Jover GarciaBristol Heart Institute, School of Clinical Sciences, University of Bristol, Bristol Royal Infirmary, Bristol, BS2 8HW, United Kingdom.
Iker Rodriguez-ArabaolazaBristol Heart Institute, School of Clinical Sciences, University of Bristol, Bristol Royal Infirmary, Bristol, BS2 8HW, United Kingdom.
Valeria AlvinoBristol Heart Institute, School of Clinical Sciences, University of Bristol, Bristol Royal Infirmary, Bristol, BS2 8HW, United Kingdom.
Elisa AvolioBristol Heart Institute, School of Clinical Sciences, University of Bristol, Bristol Royal Infirmary, Bristol, BS2 8HW, United Kingdom.
Giuseppe MangialardiBristol Heart Institute, School of Clinical Sciences, University of Bristol, Bristol Royal Infirmary, Bristol, BS2 8HW, United Kingdom.
Andrea CordaroBristol Heart Institute, School of Clinical Sciences, University of Bristol, Bristol Royal Infirmary, Bristol, BS2 8HW, United Kingdom.
Simon SatchellBristol Heart Institute, School of Clinical Sciences, University of Bristol, Bristol Royal Infirmary, Bristol, BS2 8HW, United Kingdom.
Carlo ZebeleBristol Heart Institute, School of Clinical Sciences, University of Bristol, Bristol Royal Infirmary, Bristol, BS2 8HW, United Kingdom.
Andrea CaporaliCentre for Cardiovascular Science, Queen's Medical Research Institute, Edinburgh, EH16 4TJ, United Kingdom.
Gianni AngeliniBristol Heart Institute, School of Clinical Sciences, University of Bristol, Bristol Royal Infirmary, Bristol, BS2 8HW, United Kingdom.
Paolo MadedduBristol Heart Institute, School of Clinical Sciences, University of Bristol, Bristol Royal Infirmary, Bristol, BS2 8HW, United Kingdom. mdprm@bristol.ac.uk.
Bristol Royal Infirmary · GBThe Queen's Medical Research Institute · GBUniversity of Nottingham · GB

Funding

British Heart Foundation CH/1992027/7163British Heart Foundation FS/11/52/29018British Heart Foundation PG/16/58/32275British Heart Foundation RG/13/17/30545Medical Research Council G0900912
6 · The paper itself

Abstract

Transplantation of adventitial pericytes (APCs) improves recovery from tissue ischemia in preclinical animal models by still unknown mechanisms. This study investigates the role of the adipokine leptin (LEP) in the regulation of human APC biological functions. Transcriptomic analysis of APCs showed components of the LEP signalling pathway are modulated by hypoxia. Kinetic studies indicate cultured APCs release high amounts of immunoreactive LEP following exposure to hypoxia, continuing upon return to normoxia. Secreted LEP activates an autocrine/paracrine loop through binding to the LEP receptor (LEPR) and induction of STAT3 phosphorylation. Titration studies using recombinant LEP and siRNA knockdown of LEP or LEPR demonstrate the adipokine exerts important regulatory roles in APC growth, survival, migration and promotion of endothelial network formation. Heterogeneity in LEP expression and secretion may influence the reparative proficiency of APC therapy. Accordingly, the levels of LEP secretion predict the microvascular outcome of APCs transplantation in a mouse limb ischemia model. Moreover, we found that the expression of the Lepr gene is upregulated on resident vascular cells from murine ischemic muscles, thus providing a permissive milieu to transplanted LEP-expressing APCs. Results highlight a new mechanism responsible for APC adaptation to hypoxia and instrumental to vascular repair.

Indexed as

Neovascularization, PhysiologicAdultAdventitiaAgedAnimalsAutocrine CommunicationCell HypoxiaDisease Models, AnimalFemaleFemoral ArteryGene Expression RegulationHindlimbHumansIschemiaLeptinMaleLeptinReceptors, LeptinSTAT3 Transcription Factor

Identifiers

PMID28710369
PMCPMC5511138
OpenAlexW2734527439

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.