Evidence map›Paper›PMID 30361205›Full record

ArticleBiology open2018

Hypoxia-ischemia alters distribution of lysosomal proteins in rat cortex and hippocampus.

M Troncoso, N Bannoud, L Carvelli, J Asensio, A Seltzer, M A Sosa

Abstract read
In one paragraph

Article in Biology open, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–field-weighted citation impact
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

13 citing papers in PubMed.

  1. Article
  2. Article
  3. Prosaposin in CNS health and disease, metabolic stress and exercise adaptation.Journal of molecular medicine (Berlin, Germany) · 2026
    Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Changes in the expression of the B subunit of vacuolar HIranian journal of basic medical sciences · 2021
    Article
  12. Review
  13. 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

6 authors.

M TroncosoLaboratorio de Biología y Fisiología Celular "Dr. Franciso Bertini", Instituto de Histología y Embriología - IHEM-CONICET-FCM-UNCuyo, 5500 Mendoza, Argentina.
N BannoudLaboratorio de Biología y Fisiología Celular "Dr. Franciso Bertini", Instituto de Histología y Embriología - IHEM-CONICET-FCM-UNCuyo, 5500 Mendoza, Argentina.
L CarvelliLaboratorio de Biología y Fisiología Celular "Dr. Franciso Bertini", Instituto de Histología y Embriología - IHEM-CONICET-FCM-UNCuyo, 5500 Mendoza, Argentina.
J AsensioLaboratorio de Biología y Fisiología Celular "Dr. Franciso Bertini", Instituto de Histología y Embriología - IHEM-CONICET-FCM-UNCuyo, 5500 Mendoza, Argentina.
A SeltzerLaboratorio de Biología y Fisiología Celular "Dr. Franciso Bertini", Instituto de Histología y Embriología - IHEM-CONICET-FCM-UNCuyo, 5500 Mendoza, Argentina.
M A SosaLaboratorio de Biología y Fisiología Celular "Dr. Franciso Bertini", Instituto de Histología y Embriología - IHEM-CONICET-FCM-UNCuyo, 5500 Mendoza, Argentina msosa@fcm.uncu.edu.ar.ORCID http://orcid.org/0000-0001-5579-5494

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuronal excitotoxicity induced by glutamatergic receptor overstimulation contributes to brain damage. Recent studies have shown that lysosomal membrane permeabilization (LMP) is involved in ischemia-associated neuronal death. In this study we evaluated the effect of neonatal hypoxia-ischemia (HI), as a model of excitotoxicity, on the lysosomal integrity throughout the distribution of the lysosomal proteins cathepsin D and prosaposin. Rat pups (7 days old) of the Wistar Kyoto strain were submitted to HI and they were euthanized 4 days after treatment and the cerebral cortex (Cx) and hippocampus (HIP) were processed for immunohistochemistry or immunoblotting. Treatment induced an increase of gliosis and also a redistribution of both prosaposin and cathepsin D (as intermediate and mature forms), into the cytosol of the HIP and Cx. In addition, HI induced a decrease of LAMP-1 in the membranous fraction and the appearance of a reactive band to anti-LAMP-1 in the cytosolic fraction, suggesting a cleavage of this protein. From these results, we propose that the abnormal release of Cat D and PSAP to the cytosol is triggered as a result of LAMP-1 cleavage in HI animals, which leads to cell damage. This could be a common mechanism in pathological conditions that compromises neuronal survival and brain function.

Indexed as

ExcitotoxicityHypoxia-ischemiaLysosomal enzymesLysosomes

Identifiers

PMID30361205
PMCPMC6215404

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Registered trials

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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.