Evidence map›Paper›PMID 30952817›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2019

Deletion of Biliverdin Reductase A in Myeloid Cells Promotes Chemokine Expression and Chemotaxis in Part via a Complement C5a--C5aR1 Pathway.

Kavita Bisht, Giacomo Canesin, Tasneem Cheytan, Mailin Li, Zsuzsanna Nemeth, Eva Csizmadia, Trent M Woodruff, David E Stec, Andrew C Bulmer, Leo E Otterbein and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

15 citing papers in PubMed, 19 citations in OpenAlex.

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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 5 institutions in 2 countries.

Kavita BishtDepartment of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215.ORCID 0000-0002-4073-0804
Giacomo CanesinDepartment of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215.ORCID 0000-0002-3318-4550
Tasneem CheytanDepartment of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215.
Mailin LiDepartment of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215.
Zsuzsanna NemethDepartment of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215.ORCID 0000-0003-2586-6639
Eva CsizmadiaDepartment of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215.
Trent M WoodruffSchool of Biomedical Sciences, The University of Queensland, Queensland 4072, Australia.ORCID 0000-0003-1382-911X
David E StecDepartment of Physiology and Biophysics, The University of Mississippi Medical Center, Jackson, MS 39216; and.ORCID 0000-0001-8359-4008
Andrew C BulmerSchool of Medical Science, Griffith University, Queensland 4222, Australia.
Leo E OtterbeinDepartment of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215.ORCID 0000-0002-7900-0825
Barbara WegielDepartment of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215; bwegiel@bidmc.harvard.edu.ORCID 0000-0003-0679-8765
Beth Israel Deaconess Medical Center · USGriffith University · AUThe University of Queensland · AUTranslational Research Institute · AUUniversity of Mississippi Medical Center · US

Funding

Role of biliverdin reductase during sterile inflammation in the liver.R01DK104714 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI WEGIEL, BARBARA · 2016 to 2020
$2.0M
Heme degradation pathway and immunomodulation in prostate cancer.R21CA169904 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI WEGIEL, BARBARA · 2013 to 2014
$411k
NCI NIH HHS R21 CA169904NIDDK NIH HHS R01 DK104714
6 · The paper itself

Abstract

Biliverdin reductase (BVR)-A is a pleotropic enzyme converting biliverdin to bilirubin and a signaling molecule that has cytoprotective and immunomodulatory effects. We recently showed that biliverdin inhibits the expression of complement activation fragment 5a receptor one (C5aR1) in RAW 264.7 macrophages. In this study, we investigated the role of BVR-A in determining macrophage inflammatory phenotype and function via regulation of C5aR1. We assessed expression of C5aR1, M1-like macrophage markers, including chemokines (RANTES, IP-10), as well as chemotaxis in response to LPS and C5a in bone marrow-derived macrophages from

Indexed as

AnimalsChemokinesChemotaxisComplement C5aGene DeletionMacrophagesMiceMice, TransgenicOxidoreductases Acting on CH-CH Group DonorsReceptor, Anaphylatoxin C5aSignal Transductionbiliverdin reductaseC5ar1 protein, mouseChemokinesComplement C5aOxidoreductases Acting on CH-CH Group DonorsReceptor, Anaphylatoxin C5a

Identifiers

PMID30952817
PMCPMC6504595
OpenAlexW2934656114

What OpenQuestion holds

Textmetadata
LicenceTDM
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.