Evidence map›Paper›PMID 24262755›Full record

ArticleThe American journal of pathology2014

IgE receptor-mediated mast-cell renin release.

Silvia Aldi, Pablo A Robador, Kengo Tomita, Annarita Di Lorenzo, Roberto Levi

Open access · hybridAbstract read
In one paragraph

Article in The American journal of pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
0.6field-weighted citation impact, top 31% 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

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Superantigenic Activation of Human Cardiac Mast Cells.International journal of molecular sciences · 2019
    Article
  6. Article
  7. The novel HBritish journal of pharmacology · 2016
    Article
  8. E-NTPDase1/CD39 modulates renin release from heart mast cells during ischemia/reperfusion: a novel cardioprotective role.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015
    Article
  9. 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

5 authors at 1 institution in 1 country.

Silvia AldiDepartment of Pharmacology, Weill Cornell Medical College, New York, New York.
Pablo A RobadorDepartment of Pharmacology, Weill Cornell Medical College, New York, New York.
Kengo TomitaDepartment of Pharmacology, Weill Cornell Medical College, New York, New York.
Annarita Di LorenzoDepartment of Pathology and Laboratory Medicine, Weill Cornell Medical College, New York, New York.
Roberto LeviDepartment of Pharmacology, Weill Cornell Medical College, New York, New York. Electronic address: rlevi@med.cornell.edu.
Cornell University · US

Funding

Histamine Receptor/Norepinephrine in Cardiac DysfunctionR01HL034215 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI LEVI, ROBERTO · 1985 to 2013
$6.6M
Cell-Cell Interactions in Thrombosis -Request for Extension of Merit AwardR37HL047073 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI MARCUS, AARON JACOB · 2004 to 2011
$3.7M
NHLBI NIH HHS R01 HL034215NHLBI NIH HHS R01HL034215NHLBI NIH HHS R37 HL047073NHLBI NIH HHS R37HL47073
6 · The paper itself

Abstract

Renin is a newly discovered constituent of mast cells. Given that mast cells play a major role in IgE-mediated allergic hypersensitivity, we investigated whether activation of the high-affinity IgE receptor FcεRI elicits release of mast-cell renin. Cross-linking of FcεRI on the surface of mature bone marrow-derived mast cells elicited release of enzymatically active renin protein. The angiotensin I-forming activity of the renin protein was completely blocked by the selective renin inhibitor BILA 2157, which excludes formation of angiotensin I by proteases other than renin. FcεRI-mediated mast-cell renin release was inhibited by dexamethasone and potentiated by the proinflammatory mediator PGE2. Furthermore, cross-linking of mast-cell FcεRI in ex vivo murine hearts passively sensitized with monoclonal anti-DNP IgE also resulted in mast-cell degranulation and overflow of renin. Our findings indicate that IgE-mediated allergic hypersensitivity provokes release of renin from both cultured and resident cardiac mast cells, a process likely to be exacerbated in a chronic inflammatory background. Given the widespread distribution of mast cells, and the presence of angiotensinogen and angiotensin-converting enzyme in many tissues, renin release in immediate hypersensitivity reactions could result in local angiotensin II generation and multiorgan dysfunctions.

Indexed as

AnimalsCell DegranulationCross-Linking ReagentsDexamethasoneDinoprostoneHistamineIn Vitro TechniquesMaleMast CellsMiceMice, Inbred C57BLProto-Oncogene Proteins c-kitReceptors, IgEReninCross-Linking ReagentsDexamethasoneDinoprostoneFcepsilonRIalpha protein, mouseHistamineProto-Oncogene Proteins c-kitReceptors, IgERenin

Identifiers

PMID24262755
PMCPMC3906484
OpenAlexW2084138374

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.