Evidence map›Paper›PMID 20107078›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010

BAMBI (bone morphogenetic protein and activin membrane-bound inhibitor) reveals the involvement of the transforming growth factor-beta family in pain modulation.

Mónica Tramullas, Aquilino Lantero, Alvaro Díaz, Néstor Morchón, David Merino, Ana Villar, Dirk Buscher, Ramón Merino, Juan M Hurlé, Juan Carlos Izpisúa-Belmonte and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

38 citing papers in PubMed, 63 citations in OpenAlex.

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  11. Crosstalk between Bone and Nerves within Bone.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021
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  13. Bone morphogenic protein signaling in spinal cord injury.Neuroimmunology and neuroinflammation · 2021
    Article
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  18. Defective fibrin deposition and thrombus stability in BambiJournal of thrombosis and haemostasis : JTH · 2019
    Article
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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

11 authors at 2 institutions in 2 countries.

Mónica TramullasFacultad de Medicina, Universidad de Cantabria, 39011 Santander, Spain, Instituto de Formación e Investigación Marqués de Valdecilla, 39008 Santander, Spain.
Aquilino Lantero
Alvaro Díaz
Néstor Morchón
David Merino
Ana Villar
Dirk Buscher
Ramón Merino
Juan M Hurlé
Juan Carlos Izpisúa-Belmonte
María A Hurlé
Universidad de Cantabria · ESSalk Institute for Biological Studies · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transforming growth factors-beta (TGF-betas) signal through type I and type II serine-threonine kinase receptor complexes. During ligand binding, type II receptors recruit and phosphorylate type I receptors, triggering downstream signaling. BAMBI [bone morphogenetic protein (BMP) and activin membrane-bound inhibitor] is a transmembrane pseudoreceptor structurally similar to type I receptors but lacks the intracellular kinase domain. BAMBI modulates negatively pan-TGF-beta family signaling; therefore, it can be used as an instrument for unraveling the roles of these cytokines in the adult CNS. BAMBI is expressed in regions of the CNS involved in pain transmission and modulation. The lack of BAMBI in mutant mice resulted in increased levels of TGF-beta signaling activity, which was associated with attenuation of acute pain behaviors, regardless of the modality of the stimuli (thermal, mechanical, chemical/inflammatory). The nociceptive hyposensitivity exhibited by BAMBI(-/-) mice was reversed by the opioid antagonist naloxone. Moreover, in a model of chronic neuropathic pain, the allodynic responses of BAMBI(-/-) mice also appeared attenuated through a mechanism involving delta-opioid receptor signaling. Basal mRNA and protein levels of precursor proteins of the endogenous opioid peptides proopiomelanocortin (POMC) and proenkephalin (PENK) appeared increased in the spinal cords of BAMBI(-/-). Transcript levels of TGF-betas and their intracellular effectors correlated directly with genes encoding opioid peptides, whereas BAMBI correlated inversely. Furthermore, incubation of spinal cord explants with activin A or BMP-7 increased POMC and/or PENK mRNA levels. Our findings identify TGF-beta family members as modulators of acute and chronic pain perception through the transcriptional regulation of genes encoding the endogenous opioids.

Indexed as

ActivinsAfferent PathwaysAnimalsBone Morphogenetic Protein 7Cells, CulturedDisease Models, AnimalEnkephalinsHyperalgesiaMaleMembrane ProteinsMiceMice, KnockoutNarcotic AntagonistsNociceptorsPain MeasurementPain Thresholdactivin AActivinsBambi protein, mouseBone Morphogenetic Protein 7EnkephalinsMembrane ProteinsNarcotic AntagonistsproenkephalinPro-OpiomelanocortinProtein PrecursorsReceptors, Opioid, deltaTransforming Growth Factor beta

Identifiers

PMID20107078
PMCPMC6633776
OpenAlexW2151658908

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.