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AP-1 mediates beta-amyloid-induced iNOS expression in PC12 cells via the ERK2 and p38 MAPK signaling pathways
Jang JH, Surh YJ.. Biochemical and biophysical research communications, 2005-06-01
Topic: Brain proteins, microglia and lab models
Nitrosative stress with subsequent inflammatory cell death has been implicated in some neurodegenerative disorders such as Alzheimer's disease (AD). Expression of inducible nitric oxide synthase (iNOS) and production of nitric oxide (NO) have been frequently elevated in AD. In this study, we have investigated the molecular mechanisms underlying nitrosative stress induced by beta-amyloid (A beta), a neurotoxic peptide associated with senile plaques formed in the brains of patients with AD. Exposure of rat pheochromocytoma (PC12) cells to the A beta resulted in increased mRNA and protein expression of iNOS and generation of NO. NO can rapidly interact with superoxide anion, forming more reactive peroxynitrite. Treatment of PC12 cells with A beta led to increased peroxynitrite production and nitrotyrosine formation. A beta induced activation of redox sensitive transcription factor activator protein-1 (AP-1), and AP-1 antisense oligonucleotide abolished the A beta-induced iNOS expression. Moreover, A beta transiently activated extracellular signal-regulated kinase (ERK) and p38 mitogen-activated protein kinase (p38 MAPK) via phosphorylation. Pharmacologic inhibition of both enzymes or dominant-negative mutation of ERK2 or p38 MAPK effectively down-regulated DNA binding as well as transcriptional activity of AP-1 and subsequent iNOS expression and NO production. The above findings suggest that A beta induces iNOS expression in PC12 cells through activation of AP-1 which is regulated by upstream kinases, such as ERK and p38 MAPK.
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APA 7th
Jang, J. H., & Surh, Y. J. (2005). AP-1 mediates beta-amyloid-induced iNOS expression in PC12 cells via the ERK2 and p38 MAPK signaling pathways. Biochemical and biophysical research communications. https://doi.org/10.1016/j.bbrc.2005.04.057
Vancouver
Jang JH, Surh YJ. AP-1 mediates beta-amyloid-induced iNOS expression in PC12 cells via the ERK2 and p38 MAPK signaling pathways. Biochemical and biophysical research communications. 2005. doi:10.1016/j.bbrc.2005.04.057. PMID: 15883033.
BibTeX
@article{jang2005-15883033,
author = {Jang, J. H. and Surh, Y. J.},
title = {{AP-1 mediates beta-amyloid-induced iNOS expression in PC12 cells via the ERK2 and p38 MAPK signaling pathways}},
journal = {Biochemical and biophysical research communications},
year = {2005},
doi = {10.1016/j.bbrc.2005.04.057},
pmid = {15883033},
url = {https://doi.org/10.1016/j.bbrc.2005.04.057}
}
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Key findings
- In this study, we have investigated the molecular mechanisms underlying nitrosative stress induced by beta-amyloid (A beta), a neurotoxic peptide associated with senile plaques formed in the brains of patients with AD.
- The above findings suggest that A beta induces iNOS expression in PC12 cells through activation of AP-1 which is regulated by upstream kinases, such as ERK and p38 MAPK.
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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 randomised / 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 multi-centre 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 (Biochemical and biophysical research communications) |
| 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 | 2005 — older than 20 years, still counted |
| 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) |
| Randomised / blinded | 0 / 2 | No randomisation 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 |
| Multi-centre collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 15883033) |
| 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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