ArticleMolecular medicine reports2017
Na+/K+‑ATPase DR region‑specific antibody protects U251 cells against hypoxia reperfusion‑induced injury via the PI3K/AKT and ERK pathways.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 4 papers.
What it found
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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.
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.
Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- Mechanisms of glutamate metabolic function and dysfunction in vascular dementia.Neuroprotection (Chichester, England) · 2024Review
- Role of NaJournal of molecular medicine (Berlin, Germany) · 2022Review
- DR-region of NaCell death & disease · 2018Article
- High Expression of ABL2 Suppresses Apoptosis in Gastric Cancer.Digestive diseases and sciences · 2018Article
Corrections and comments
- Retracted[Retracted] Na2026
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cerebral ischemia is a condition in which there is insufficient blood flow to the brain to meet metabolic demand. This leads to poor oxygen supply or cerebral hypoxia and to the death of brain tissue or cerebral infarction/ischemic stroke. In the present study, an Na+/K+‑ATPase (NKA) DR region‑specific antibody (DRSAb) was established and purified and it was demonstrated that DRSAb induced a protective effect on human astrocytes (U251) via the phosphoinositide 3‑kinase (PI3K)/AKT and extracellular signal‑regulated protein kinase (ERK) signaling pathways. The binding of DRSAb on NKA was revealed using flow cytometry. High signals were detected on U251 cells incubated with DRSAb, but not with control sera or BSA. The viability of the hypoxia/reperfusion (H/R)‑treated cells was markedly increased by DRSAb administration of 0.3‑0.5 µM. The optimal concentration of DRSAb was 0.4 µM for attenuation of the injury induced by H/R. The administration of 0.4 µM DRSAb markedly reduced the number of apoptotic cells compared with control sera. The application of PD98059, an ERK inhibitor, and LY‑294002, an AKT inhibitor, attenuated the protective effect induced by DRSAb in the U251 cells subjected to H/R. Furthermore, the application of LY294002 prior to incubation with DRSAb eliminated the activation of ERK1/2, whereas the use of PD98059 failed to attenuate the effect of DRSAb on PI3K/AKT activation. These results indicated that the protective effects of DRSAb against H/R injury in U251 cells occurred via stimulation of the PI3K/AKT and ERK signaling pathways.
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Registered trials
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.