Evidence map›Paper›PMID 20981579›Full record

ArticleJournal of molecular neuroscience : MN2011

Potential protective role of IL15Rα during inflammation.

Weihong Pan, Xiaojun Wu, Abba J Kastin, Yan Zhang, Hung Hsuchou, Franz Halberg, Finla Chatu, Reas S Khan, Barry Robert, Germaine G Cornelissen-Guillaume

Abstract read
In one paragraph

Article in Journal of molecular neuroscience : MN, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.6field-weighted citation impact, top 33% 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, 11 citations in OpenAlex.

  1. Review
  2. Review
  3. Diminished leptin signaling can alter circadian rhythm of metabolic activity and feeding.Journal of applied physiology (Bethesda, Md. : 1985) · 2013
    Article
  4. Endothelial leptin receptor mutation provides partial resistance to diet-induced obesity.Journal of applied physiology (Bethesda, Md. : 1985) · 2012
    Article
  5. Article
  6. Article
  7. NFĸB is an unexpected major mediator of interleukin-15 signaling in cerebral endothelia.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2011
    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

10 authors at 2 institutions in 1 country.

Weihong PanBlood-Brain Barrier Group, Pennington Biomedical Research Center, 6400 Perkins Road, Baton Rouge, LA 70808, USA. weihong.pan@pbrc.edu
Xiaojun Wu
Abba J Kastin
Yan Zhang
Hung Hsuchou
Franz Halberg
Finla Chatu
Reas S Khan
Barry Robert
Germaine G Cornelissen-Guillaume
Pennington Biomedical Research Center · USUniversity of Minnesota · US

Funding

Leptin Transport Across the BBB: The Role of ObR (+) AstrocytesR01DK054880 · NIDDK · TULANE UNIVERSITY OF LOUISIANA · PI KASTIN, ABBA J · 1999 to 2014
$4.4M
Neuroimmune modulation across the BBB: Regulation of ILS trafficking by TNFR01NS062291 · NINDS · LSU PENNINGTON BIOMEDICAL RESEARCH CTR · PI PAN, WEIHONG · 2008 to 2012
$1.6M
Consequences of Astrocytic Leptin Receptor Upregulation on ObesityR01DK092245 · NIDDK · LSU PENNINGTON BIOMEDICAL RESEARCH CTR · PI KASTIN, ABBA J · 2011 to 2014
$1.3M
Transport of TNFalpha across the BBBR01NS045751 · NINDS · TULANE UNIVERSITY OF LOUISIANA · PI PAN, WEIHONG · 2004 to 2008
$1.1M
TIMING OF PHYSIOLOGIC FUNCTIONS IN HEALTH AND DISEASEK06GM013981 · NIGMS · UNIVERSITY OF MINNESOTA TWIN CITIES · PI HALBERG, FRANZ · 1985 to 2012
$424k
Leptin Transport across the BBB: The Role of ObR (+) astrocytesR56DK054880 · NIDDK · LSU PENNINGTON BIOMEDICAL RESEARCH CTR · PI KASTIN, ABBA J · 2010 to 2010
$222k
NIDDK NIH HHS DK54880NIDDK NIH HHS R01 DK054880NIDDK NIH HHS R01 DK092245NIDDK NIH HHS R56 DK054880NIGMS NIH HHS K06 GM013981NINDS NIH HHS NS45751NINDS NIH HHS NS62291NINDS NIH HHS R01 NS045751NINDS NIH HHS R01 NS062291
6 · The paper itself

Abstract

We have shown that TNFα specifically activates the interleukin-15 (IL15) system in cerebral endothelial cells composing the blood-brain barrier. To determine the functions of cerebral IL15 signaling in inflammation, we first treated mice with lipopolysaccharide (LPS) and determined the expression of the three receptor subtypes of IL15. Robust time-dependent upregulation occurred in all subunits. We then tested whether IL15Rα knockout (KO) affected the maintenance of body temperature and activity level after a single dose of LPS. Circadian telemetry data were analyzed by the cosinor method. Both wild-type and KO mice had clear 24-h rhythms of basal temperature and activity. KO mice had a significantly higher midline estimating statistic of rhythm (MESOR; approximating 24 h mean) of temperature and delayed 24-h acrophase (peak) of activity than the wild-type mice. LPS disrupted the circadian rhythm of activity more severely in the KO group. Besides a decrease in MESOR and 24-h amplitude of activity after LPS, the KO mice showed a significant reduction of MESOR, amplitude, and changed acrophase for temperature on the second of 2 days. The disrupted circadian rhythm of temperature and activity in the KO mice after LPS suggests that upregulated IL15 receptors may serve a beneficial role to counteract the consequences of neuroinflammation.

Indexed as

AnimalsBody TemperatureCentral Nervous SystemCircadian RhythmInflammationInterleukin-15 Receptor alpha SubunitLipopolysaccharidesMiceMice, KnockoutMotor ActivityProtein IsoformsTelemetryInterleukin-15 Receptor alpha SubunitLipopolysaccharidesProtein Isoforms

Identifiers

PMID20981579
PMCPMC3521591
OpenAlexW1996605358

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.