Evidence map›Paper›PMID 23132855›Full record

ArticleThe Journal of biological chemistry2012

Kinin-B2 receptor activity determines the differentiation fate of neural stem cells.

Cleber A Trujillo, Priscilla D Negraes, Telma T Schwindt, Claudiana Lameu, Cassiano Carromeu, Alysson R Muotri, João B Pesquero, Débora M Cerqueira, Micheli M Pillat, Héllio D N de Souza and 3 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

22 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
  2. Activation of Bradykinin BInternational journal of molecular sciences · 2024
    Article
  3. Article
  4. Article
  5. Article
  6. Neuropathic pain in patients with post-COVID-19.Northern clinics of Istanbul · 2023
    Article
  7. Article
  8. Article
  9. Article
  10. Kinins in Glioblastoma Microenvironment.Cancer microenvironment : official journal of the International Cancer Microenvironment Society · 2019
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
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  18. Article
  19. Article
  20. Review
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

13 authors at 4 institutions in 2 countries.

Cleber A TrujilloDepartamento de Bioquímica, Instituto de Química, Universidade de São Paulo, São Paulo, Brazil 05508-000.
Priscilla D Negraes
Telma T Schwindt
Claudiana Lameu
Cassiano Carromeu
Alysson R Muotri
João B Pesquero
Débora M Cerqueira
Micheli M Pillat
Héllio D N de Souza
Lauro T Turaça
José G Abreu
Henning Ulrich
Universidade de São Paulo · BRUniversidade Federal de São Paulo · BRUniversidade Federal do Rio de Janeiro · BRUniversity of California, San Diego · US

Funding

Modeling autism with human pluripotent cellsDP2OD006495 · OD · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MUOTRI, ALYSSON R. · 2009 to 2009
$2.3M
NIH HHS 1-DP2-OD006495-01NIH HHS DP2 OD006495
6 · The paper itself

Abstract

Bradykinin is not only important for inflammation and blood pressure regulation, but also involved in neuromodulation and neuroprotection. Here we describe novel functions for bradykinin and the kinin-B2 receptor (B2BkR) in differentiation of neural stem cells. In the presence of the B2BkR antagonist HOE-140 during rat neurosphere differentiation, neuron-specific β3-tubulin and enolase expression was reduced together with an increase in glial protein expression, indicating that bradykinin-induced receptor activity contributes to neurogenesis. In agreement, HOE-140 affected in the same way expression levels of neural markers during neural differentiation of murine P19 and human iPS cells. Kinin-B1 receptor agonists and antagonists did not affect expression levels of neural markers, suggesting that bradykinin-mediated effects are exclusively mediated via B2BkR. Neurogenesis was augmented by bradykinin in the middle and late stages of the differentiation process. Chronic treatment with HOE-140 diminished eNOS and nNOS as well as M1-M4 muscarinic receptor expression and also affected purinergic receptor expression and activity. Neurogenesis, gliogenesis, and neural migration were altered during differentiation of neurospheres isolated from B2BkR knock-out mice. Whole mount in situ hybridization revealed the presence of B2BkR mRNA throughout the nervous system in mouse embryos, and less β3-tubulin and more glial proteins were expressed in developing and adult B2BkR knock-out mice brains. As a underlying transcriptional mechanism for neural fate determination, HOE-140 induced up-regulation of Notch1 and Stat3 gene expression. Because pharmacological treatments did not affect cell viability and proliferation, we conclude that bradykinin-induced signaling provides a switch for neural fate determination and specification of neurotransmitter receptor expression.

Indexed as

Cell DifferentiationAnimalsCells, CulturedFemaleHumansMaleMiceMice, Inbred C57BLMice, KnockoutNeural Stem CellsRatsRats, WistarReceptor, Bradykinin B2Signal TransductionReceptor, Bradykinin B2

Identifiers

PMID23132855
PMCPMC3531721
OpenAlexW2058471388

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.