Evidence map›Paper›PMID 19443690›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2009

Neurotensin induces IL-6 secretion in mouse preadipocytes and adipose tissues during 2,4,6,-trinitrobenzensulphonic acid-induced colitis.

Hon-Wai Koon, You Sun Kim, Hua Xu, Aatish Kumar, Dezheng Zhao, Iordanes Karagiannides, Paul R Dobner, Charalabos Pothoulakis

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.0field-weighted citation impact, top 16% 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

33 citing papers in PubMed, 65 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. New Insights in the Control of Fat Homeostasis: The Role of Neurotensin.International journal of molecular sciences · 2022
    Review
  6. Article
  7. Article
  8. Absence of neurotensin attenuates intestinal dysbiosis and inflammation by maintaining Mmp7/α-defensin axis in diet-induced obese mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Article
  9. Article
  10. The emerging role of lncRNAs in inflammatory bowel disease.Experimental & molecular medicine · 2018
    Review
  11. Article
  12. Article
  13. Article
  14. Role of G protein-coupled receptors-microRNA interactions in gastrointestinal pathophysiology.American journal of physiology. Gastrointestinal and liver physiology · 2017
    Review
  15. Article
  16. The Role of Neuropeptides in Mouse Models of Colitis.Journal of molecular neuroscience : MN · 2016
    Review
  17. Article
  18. Article
  19. Article
  20. 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

8 authors at 5 institutions in 2 countries.

Hon-Wai KoonDivision of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA.
You Sun Kim
Hua Xu
Aatish Kumar
Dezheng Zhao
Iordanes Karagiannides
Paul R Dobner
Charalabos Pothoulakis
University of California, Los Angeles · USBeth Israel Deaconess Medical Center · USHarvard University · USInje University Seoul Paik Hospital · KRUniversity of Massachusetts Chan Medical School · US

Funding

Mechanisms of Neurotensin in Intestinal InflammationR01DK060729 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI POTHOULAKIS, CHARALABOS · 2002 to 2017
$5.0M
NIDDK NIH HHS DK060729NIDDK NIH HHS R01 DK060729
6 · The paper itself

Abstract

Mesenteric fat is known to undergo inflammatory changes after 2,4,6,-trinitrobenzensulphonic acid (TNBS)-induced colitis. Neurotensin (NT) and neurotensin receptor 1 (NTR1) have been shown to play a major role in the pathogenesis of intestinal inflammation. This led us to explore whether NT and NTR1 are expressed in the mesenteric fat depots during TNBS-induced colitis and whether NT participates in the increased interleukin (IL)-6 secretion in this inflammatory response. TNBS-induced inflammation in the colon increases NT and NTR1 expression in mesenteric adipose tissues, including mesenteric preadipocytes. Compared with wild-type mice, NT knockout (KO) mice have reduced TNBS-induced colitis accompanied by diminished inflammatory responses in mesenteric adipose tissue. Specifically, IL-6 and p65 phosphorylation levels in mesenteric fat of NT KO mice are also reduced compared with wild-type mice. Mouse 3T3-L1 preadipocytes express NTR1 and its expression is increased after stimulation of preadipocytes with proinflammatory cytokines. NT stimulation of 3T3-L1 preadipocytes overexpressing NTR1 causes PKCdelta phosphorylation and IL-6 secretion in a time- and dose-dependent fashion. Moreover, NT-mediated IL-6 expression is nuclear factor-kappaB and PKCdelta dependent. We also found that supernatants from NT-exposed 3T3-L1-NTR1 preadipocytes and mesenteric fat obtained from wild-type mice 2 days after TNBS administration stimulate an IL-6-dependent macrophage migration measured by a macrophage migration assay, whereas this response is reduced when mesenteric fat from NT KO mice is used. These results demonstrate an important role for NT in acute colitis and adipose tissue inflammation associated with experimental colitis that involves direct NT proinflammatory responses in preadipocytes.

Indexed as

3T3-L1 CellsAdipocytesAdipose TissueAnimalsCell DifferentiationCell MovementColitisInterleukin-6MacrophagesMiceMice, KnockoutNeurotensinNF-kappa BPhosphorylationProtein Kinase C-deltaProtein SubunitsInterleukin-6Neurotensinneurotensin type 1 receptorNF-kappa BProtein Kinase C-deltaProtein SubunitsReceptors, NeurotensinTrinitrobenzenesulfonic Acid

Identifiers

PMID19443690
PMCPMC2688970
OpenAlexW2016129079

What OpenQuestion holds

Textmetadata
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.