Evidence map›Paper›PMID 21436843›Full record

ArticleCell death and differentiation2011

Autophagy, and BiP level decrease are early key events in retrograde degeneration of motoneurons.

C Penas, M Font-Nieves, J Forés, V Petegnief, A Planas, X Navarro, C Casas

Open access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 2 pooled it
3.0field-weighted citation impact, top 9% 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

40 citing papers in PubMed, 2 syntheses or guidelines pooled it, 56 citations in OpenAlex.

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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

7 authors at 5 institutions in 1 country.

C PenasGroup of Neuroplasticity and Regeneration, Institute of Neurosciences, Department of Cell Biology, Physiology and Immunology, Universitat Autònoma de Barcelona, and Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Spain.
M Font-Nieves
J Forés
V Petegnief
A Planas
X Navarro
C Casas
Biomedical Research Networking Center on Neurodegenerative Diseases · ESConsorci Institut D'Investigacions Biomediques August Pi I Sunyer · ESCentro de Investigación Biomédica en Red · ESInstitut d'Investigacions Biomèdiques de Barcelona · ESUniversitat de Barcelona · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Disconnection of the axon from the soma of spinal motoneurons (MNs) leads either to a retrograde degenerative process or to a regenerative reaction, depending on the severity and the proximity to the soma of the axonal lesion. The endoplasmic reticulum (ER) is a continuous membranous network that extends from the nucleus to the entire cytoplasm of the neuronal soma, axon and dendrites. We investigated whether axonal injury is sensed by the ER and triggers the activation of protective mechanisms, such as the unfolded protein response (UPR) and autophagy. We found early (at 3 days) accumulation of beclin1, LC3II and Lamp-1, hallmarks of autophagy, in both degenerating MNs after spinal root avulsion and in non-degenerating MNs after distal nerve section, although Lamp-1 disappeared by 5 days only in the former. In contrast, only degenerating MNs presented early activation of IRE1α, revealed by an increase of the spliced isoform of Xbp1 and accumulation of ATF4 in their nucleus, two branches of the UPR, and late BiP downregulation in association with cytoskeletal and organelle disorganization. We conclude that BiP decrease is a signature of the degenerating process, as its overexpression led to an increase in MN survival after root avulsion. Besides, Bcl2 is strongly implicated in the survival pathway activated by BiP overexpression.

Indexed as

Activating Transcription Factor 4AnimalsApoptosis Regulatory ProteinsAutophagyBeclin-1Blotting, WesternDNA-Binding ProteinsEndoplasmic ReticulumEndoplasmic Reticulum Chaperone BiPFemaleHeat-Shock ProteinsImmunohistochemistryLysosomal-Associated Membrane Protein 1Lysosomal Membrane ProteinsMotor NeuronsRatsActivating Transcription Factor 4Apoptosis Regulatory ProteinsAtf4 protein, ratBeclin-1Becn1 protein, ratDNA-Binding ProteinsEndoplasmic Reticulum Chaperone BiPGRP78 protein, ratHeat-Shock ProteinsLamp1 protein, ratLysosomal-Associated Membrane Protein 1Lysosomal Membrane ProteinsRegulatory Factor X Transcription FactorsTranscription FactorsX-Box Binding Protein 1Xbp1 protein, rat

Identifiers

PMID21436843
PMCPMC3172115
OpenAlexW2058663392

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.