Evidence map›Paper›PMID 26983718›Full record

ArticleCellular and molecular neurobiology2017

Time-Dependent Changes in Apoptosis Upon Autophagy Inhibition in Astrocytes Exposed to Oxygen and Glucose Deprivation.

Daniela Kasprowska, Grzegorz Machnik, Alicja Kost, Bożena Gabryel

Open access · greenAbstract read
In one paragraph

Article in Cellular and molecular neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

19 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
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  7. The Role of Circular RNAs in Ischemic Stroke.Neurochemical research · 2023
    Review
  8. Article
  9. Article
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  12. Review
  13. Article
  14. Article
  15. Autophagy and inflammation in ischemic stroke.Neural regeneration research · 2020
    Review
  16. Article
  17. Article
  18. Review
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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

4 authors at 1 institution in 1 country.

Daniela KasprowskaDepartment of Pharmacology, School of Medicine in Katowice, Medical University of Silesia, Medyków 18, 40-752, Katowice, Poland. d.kasprowska@awf.katowice.pl.
Grzegorz MachnikDepartment of Internal Medicine and Clinical Pharmacology, School of Medicine in Katowice, Medical University of Silesia, Medyków 18, 40-752, Katowice, Poland.
Alicja KostDepartment of Histology, School of Medicine in Katowice, Medical University of Silesia, Medyków 18, 40-752, Katowice, Poland.
Bożena GabryelDepartment of Pharmacology, School of Medicine in Katowice, Medical University of Silesia, Medyków 18, 40-752, Katowice, Poland.
Medical University of Silesia · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent studies have implicated the role of autophagy in brain ischemia pathophysiology. However, it remains unclear whether autophagy activation is protective or detrimental to astrocytes undergoing ischemic stress. This study evaluated the influence of ischemia-induced autophagy on cell death and the course of intrinsic and extrinsic apoptosis in primary cultures of rat cortical astrocytes exposed to combined oxygen-glucose deprivation (OGD). The role of autophagy was assessed by pharmacological inhibition with 3-methyladenine (3-MA). Cell viability was evaluated by measuring LDH release and through the use of the alamarBlue Assay. Apoptosis and necrosis were determined by fluorescence microscopy after Hoechst 33,342 and propidium iodide staining, respectively. The levels of apoptosis-related proteins were analyzed by immunoblotting. The downregulation of autophagy during OGD resulted in decreased cell viability and time-dependent changes in levels of apoptosis and necrosis. After short-term OGD (1, 4 h), cells treated with 3-MA showed higher level of cleaved caspase 3 compared with control cells. This result was consistent with an evaluation of apoptotic cell number by fluorescence microscopy. However, after prolonged exposure to OGD (8, 24 h), the number of apoptotic astrocytes (microscopically evaluated) did not differ or was even lower (as marked by caspase 3) in the presence of the autophagy inhibitor in comparison to the control. A higher level of necrosis was observed in 3-MA-treated cells compared to non-treated cells after 24 h OGD. The downregulation of autophagy caused time-dependent changes in both extrinsic (cleaved caspase 8, TNFα) and intrinsic (cleaved caspase 9) apoptotic pathways. Our results strongly indicate that the activation of autophagy in astrocytes undergoing ischemic stress is an adaptive mechanism, which allows for longer cell survival by delaying the initiation of apoptosis and necrosis.

Indexed as

AdenineAnimalsAnimals, NewbornApoptosisAstrocytesAutophagyCell HypoxiaCells, CulturedCerebral CortexGlucoseRatsRats, WistarTime Factors3-methyladenineAdenineGlucoseApoptosisAstrocyteAutophagyIschemia

Identifiers

PMID26983718
PMCPMC11482150
OpenAlexW2298860825

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.