Evidence map›Paper›PMID 27076683›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2016

Neurotensin Promotes the Development of Colitis and Intestinal Angiogenesis via Hif-1α-miR-210 Signaling.

Kyriaki Bakirtzi, Ivy Ka Man Law, Xiang Xue, Dimitrios Iliopoulos, Yatrik M Shah, Charalabos Pothoulakis

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.5field-weighted citation impact, top 12% 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

29 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
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  10. Review
  11. Epigenetics of Inflammatory Bowel Diseases.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2023
    Article
  12. Article
  13. Article
  14. Protective Effect ofOxidative medicine and cellular longevity · 2022
    Article
  15. Neuroimmunomodulation by gut bacteria: Focus on inflammatory bowel diseases.World journal of gastrointestinal pathophysiology · 2021
    Review
  16. Article
  17. Article
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  19. Review
  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

6 authors at 2 institutions in 1 country.

Kyriaki BakirtziInflammatory Bowel Disease Center, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095;ORCID 0000-0003-1535-2490
Ivy Ka Man LawInflammatory Bowel Disease Center, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095;ORCID 0000-0002-7430-1215
Xiang XueDivision of Gastroenterology, Department of Molecular and Integrative Physiology, University of Michigan Medical School, Ann Arbor, MI 48109;ORCID 0000-0003-4704-1814
Dimitrios IliopoulosDivision of Digestive Diseases, Center for Systems Biomedicine, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095; and.ORCID 0000-0002-6832-0786
Yatrik M ShahDivision of Gastroenterology, Department of Molecular and Integrative Physiology, University of Michigan Medical School, Ann Arbor, MI 48109; Division of Gastroenterology, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI 48109.
Charalabos PothoulakisInflammatory Bowel Disease Center, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095; cpothoulakis@mednet.ucla.edu.
University of California, Los Angeles · USUniversity of Michigan · US

Funding

Pilot and Feasibility ProgramP30DK041301 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ROZENGURT, JUAN ENRIQUE · 1990 to 2019
$18.0M
Women's Health and Functional Visceral Disorders CenterP50DK064539 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI MAYER, EMERAN A · 2002 to 2017
$17.5M
Control of iron absorption by intestinal HIF2 in iron and hematological disordersR01DK095201 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SHAH, YATRIK M · 2012 to 2025
$5.7M
The role of HIF2alpha in colon carcinogenesisR01CA148828 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SHAH, YATRIK M · 2010 to 2025
$5.2M
Mechanisms of Neurotensin in Intestinal InflammationR01DK060729 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI POTHOULAKIS, CHARALABOS · 2002 to 2017
$5.0M
NCI NIH HHS R01 CA148828NIDDK NIH HHS P30 DK041301NIDDK NIH HHS P50 DK064539NIDDK NIH HHS R01 DK060729NIDDK NIH HHS R01 DK095201
6 · The paper itself

Abstract

Neurotensin (NT) via its receptor 1 (NTR1) modulates the development of colitis, decreases HIF-1α/PHD2 interaction, stabilizes and increases HIF-1α transcriptional activity, and promotes intestinal angiogenesis. HIF-1α induces miR-210 expression, whereas miR-210 is strongly upregulated in response to NT in NCM460 human colonic epithelial cells overexpressing NTR1 (NCM460-NTR1). In this study, we examined whether NT activates a NTR1-HIF-1α-miR-210 cascade using in vitro (NCM460-NTR1 cells) and in vivo (transgenic mice overexpressing [HIF-1α-OE] or lacking HIF-1α [HIF-1α-knockout (KO)] in intestinal epithelial cells and mice lacking NTR1 [NTR1-KO]) models. Pretreatment of NCM460-NTR1 cells with the HIF-1α inhibitor PX-478 or silencing of HIF-1α (small interfering HIF-1α) attenuated miR-210 expression in response to NT. Intracolonic 2,4,6-trinitrobenzenesulfonic acid (TNBS) administration (2-d model) increased colonic miR-210 expression that was significantly reduced in NTR1-KO, HIF-1α-KO mice, and wild-type mice pretreated intracolonically with locked nucleic acid anti-miR-210. In contrast, HIF-1α-OE mice showed increased miR-210 expression at baseline that was further increased following TNBS administration. HIF-1α-OE mice had also exacerbated TNBS-induced neovascularization compared with TNBS-exposed wild-type mice. TNBS-induced neovascularization was attenuated in HIF-1α-KO mice, or mice pretreated intracolonically with anti-miR-210. Intracolonic anti-miR-210 also reduced colitis in response to TNBS (2 d). Importantly, miR-210 expression was increased in tissue samples from ulcerative colitis patients. We conclude that NT exerts its proinflammatory and proangiogenic effects during acute colitis via a NTR1-prolyl hydroxylase 2/HIF-1α-miR-210 signaling pathway. Our results also demonstrate that miR-210 plays a proinflammatory role in the development of colitis.

Indexed as

AnimalsCell Line, TumorColitis, UlcerativeColonEpithelial CellsHumansHypoxia-Inducible Factor 1, alpha SubunitIntestinal MucosaMaleMiceMice, Inbred C57BLMice, KnockoutMicroRNAsMustard CompoundsNeovascularization, PathologicNeurotensin2-amino-3-(4'-N,N-bis(2-chloroethyl)amino)phenylpropionic acid N-oxideHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitMicroRNAsMIRN210 microRNA, humanMustard CompoundsNeurotensinneurotensin type 1 receptorNF-kappa BPhenylpropionatesReceptors, NeurotensinTrinitrobenzenesulfonic Acid

Identifiers

PMID27076683
PMCPMC4868643
OpenAlexW2339513854

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.