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Record W2073254446 · doi:10.1016/j.jalz.2012.05.819

P2‐114: Extracellular mitochondrial transcription factor A (Tfam) as a potential signaling molecule that promotes inflammation and induces microglia‐mediated neurotoxicity

2012· article· en· W2073254446 on OpenAlexaff
Jonathan P. Little, Jocelyn M. Madeira, Manpreet Bahniwal, Kirsten R. Wolthers, Andis Klegeris

Bibliographic record

VenueAlzheimer s & Dementia · 2012
Typearticle
Languageen
FieldNeuroscience
TopicNeuroinflammation and Neurodegeneration Mechanisms
Canadian institutionsOkanagan University CollegeUniversity of British Columbia, Okanagan CampusUniversity of British Columbia
Fundersnot available
KeywordsTFAMMicrogliaNeuroinflammationInflammationCell biologyBiologyChemokineMolecular biologyImmunologyMitochondrionCancer researchMitochondrial biogenesis

Abstract

fetched live from OpenAlex

Recent findings indicate that mitochondrial proteins released from injured or dying cells contain damage associated molecular patterns (DAMPs) that activate innate immune responses and promote inflammation in peripheral tissues. Given that chronic brain inflammation is linked to neuronal death in Alzheimer's disease (AD), we explored a potential role for mitochondrial DAMPs as signaling molecules that could activate microglia. Human THP-1 monocytic cells and peripheral blood mononuclear cells (PBMCs) prepared from healthy human donors were used to model microglia. An established cell culture model of neuroinflammation involving transfer of conditioned media from monocytic cells to human SH-SY5Y neuroblastoma cells was used to examine whether mitochondrial proteins promoted inflammation and caused monocyte-mediated neurotoxicity. In order to further explore specific mitochondrial proteins responsible for inducing inflammation, we made and tested purified recombinant human mitochondrial transcription factor A (Tfam), which is the mitochondrial homologue of high-mobility group box (HMGB1), a nuclear transcription factor recently implicated in neuroinflammation. Pro-inflammatory cytokine mRNA expression in THP-1 cells exposed to Tfam was also assessed by quantitative real-time PCR. Conditioned media from THP-1 cells stimulated for 48 h with isolated mitochondrial proteins (50-100 μg/ml) or Tfam (1.25-5 μg/ml) combined with interferon (IFN)-γ (150 U/ml) induced SH-SY5Y neuroblastoma cell death, which could be detected after 72 h incubation by the MTT assay (P<0.05). Tfam combined with IFN-γ also induced neurotoxic secretions from PBMCs. Tfam upregulated mRNA expression of interleukin (IL)-1β, IL-6, and IL-8 in THP-1 cells (P<0.05), an effect that was augmented (P<0.05) by costimulation with IFN-γ. Tfam was not directly cytotoxic to THP-1 or SH-SY5Y cells. Heating (95°C for 10 min) Tfam prior to stimulation of THP-1 cells significantly reduced its activity (P<0.05), while pre-treatment with polymixin B had no effect, indicating that the effects observed by using the recombinant protein were not due to endotoxin contamination. These findings indicate that mitochondrial DAMPS, in particular Tfam, could be detected by mononuclear phagocytes including microglia and have the potential to induce their neurotoxicity and pro-inflammatory cytokine secretion. Whether Tfam or other mitochondrial proteins released from damaged or dying neurons promote neuroinflammation in AD brain remains to be determined.

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

How this classification was reachedexpand

Full frame machine prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.

metaresearch head score (Codex)0.000
metaresearch head score (Gemma)0.000
Version: metacan-v3-hybrid-931329e0061cValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Bench or experimental · Consensus signal: Bench or experimental
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.002
Threshold uncertainty score0.008

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0000.000
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0000.000
Science and technology studies0.0000.000
Scholarly communication0.0000.000
Open science0.0000.000
Research integrity0.0010.001
Insufficient payload (model declined to judge)0.0020.001

Machine scores (provisional)

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

Opus teacher head0.047
GPT teacher head0.256
Teacher spread0.209 · how far apart the two teachers sit on this one work
Validation statusscore_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Classification

machine, unvalidated

Machine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.

The models applied no category: nothing in the taxonomy fit this work.
Study designBench or experimental
Domainnot available
GenreEmpirical

How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".

Quick stats

Citations0
Published2012
Admission routes1
Has abstractyes

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