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Erythropoietin protects PC12 cells from beta-amyloid(25-35)-induced apoptosis via PI3K/Akt signaling pathway
Ma R, Ma R, Xiong N, Huang C, Tang Q, Hu B, Xiang J, Li G.. Neuropharmacology, 2009-03-04
Topic: Brain proteins, microglia and lab models
Plain-language summary
Although the etiology of Alzheimer's disease (AD) is not fully understood, multiple lines of evidence suggests the importance of amyloid-beta (Abeta) in the initiation/progression of the disease. In this study, we investigated protective effects of erythropoietin (EPO) on Abeta(25-35)-induced cell death in cultured rat pheochromocytoma cells (PC12 cells). EPO (2U/ml) in combination with Abeta(25-35) increased the cell viability and reduced the number of apoptotic cells by MTT assay, Trypan blue dye exclusion method, TUNEL staining and Hoechst 33342 staining. In mechanistic study, EPO induced time-dependent phosphorylation of phosphatidylinositol 3-kinase (PI3K) substrate Akt. Treatment of PC12 cells with PI3K inhibitors LY294002 abolished the protective effects of EPO. EPO also induced the phosphorylation of glycogen synthase kinase-3beta (GSK-3beta), a downstream target of PI3K/Akt, and GSK-3beta inhibitors lithium chloride blocked Abeta(25-35)-induced cell apoptosis in a manner similar to EPO, suggesting that GSK-3beta inhibition is involved in EPO-mediated cytoprotection. Moreover, the expression of anti-apoptotic protein Bcl-2 was increased by EPO involving PI3K/Akt pathway. These studies demonstrate that EPO is an effective neuroprotective agent and is a viable candidate for treating AD.
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APA 7th
Ma, R., Xiong, N., Huang, C., Tang, Q., Hu, B., Xiang, J., et al. (2009). Erythropoietin protects PC12 cells from beta-amyloid(25-35)-induced apoptosis via PI3K/Akt signaling pathway. Neuropharmacology. https://doi.org/10.1016/j.neuropharm.2009.02.006
Vancouver
Ma R, Xiong N, Huang C, Tang Q, Hu B, Xiang J, et al. Erythropoietin protects PC12 cells from beta-amyloid(25-35)-induced apoptosis via PI3K/Akt signaling pathway. Neuropharmacology. 2009. doi:10.1016/j.neuropharm.2009.02.006. PMID: 19268480.
BibTeX
@article{ma2009-19268480,
author = {Ma, R. and Xiong, N. and Huang, C. and Tang, Q. and Hu, B. and Xiang, J. and Li, G.},
title = {{Erythropoietin protects PC12 cells from beta-amyloid(25-35)-induced apoptosis via PI3K/Akt signaling pathway}},
journal = {Neuropharmacology},
year = {2009},
doi = {10.1016/j.neuropharm.2009.02.006},
pmid = {19268480},
url = {https://doi.org/10.1016/j.neuropharm.2009.02.006}
}
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. The record names 7 authors; APA and Vancouver show the first six, BibTeX and the downloads carry all of them. Check the citation against the original before you use it.
Key findings
- EPO also induced the phosphorylation of glycogen synthase kinase-3beta (GSK-3beta), a downstream target of PI3K/Akt, and GSK-3beta inhibitors lithium chloride blocked Abeta(25-35)-induced cell apoptosis in a manner similar to EPO, suggesting that GSK-3beta inhibition is involved in EPO-mediated cytoprotection.
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Study details
- Evidence strengthLow
How this study scored 36/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomized / blinded because the record does not state it. We have no data on journal's citation record, times cited, citations per year, impact for its field and year, cited by studies here, still being cited, senior author's track record, institution's track record and multicenter collaboration, so those were left out: it earned 21 of the 58 points we could judge it on, which is 36 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Neuropharmacology) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 1 / 5 | 2009 — within 20 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | — / 7 | No citation count (not found in OpenAlex) — left out of this score |
| Citations per year | — / 5 | No citation count or no year — left out of this score |
| Impact for its field and year | — / 6 | No field-weighted citation impact (OpenAlex has none yet) — left out of this score |
| Cited by studies here | — / 6 | Not yet checked against this library's citation graph — left out of this score |
| Still being cited | — / 4 | No yearly citation counts — left out of this score |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| Institution's track record | — / 3 | No institution listed in OpenAlex — left out of this score |
| Multicenter collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 19268480) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 21 / 58 | Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 21 of the 58 points we could judge it on is 36 out of 100. |
| Total | 36 / 100 | — |
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