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RIPK3-Mediated Necroptosis Regulates Cardiac Allograft Rejection.

2014· article· en· W2772426703 on OpenAlexaff
Alexander Pavlosky, Arthur Lau, Aaron Haig, Z. Zhang, Anthony M. Jevnikar

Bibliographic record

VenueTransplantation · 2014
Typearticle
Languageen
FieldBiochemistry, Genetics and Molecular Biology
TopicCell death mechanisms and regulation
Canadian institutionsLondon Health Sciences Centre
Fundersnot available
KeywordsNecroptosisRIPK1Programmed cell deathTransplantationApoptosisTumor necrosis factor alphaNecrosisChemistryCancer researchImmunologyCell biologyMedicineBiologyPathologyBiochemistryInternal medicine

Abstract

fetched live from OpenAlex

Previous studies have shown that Tumour Necrosis Factor Alpha (TNFα) contributes to cell death by activating apoptotic and newly identified Receptor Interacting Protein Kinase 1 and 3 (RIPK1/RIPK3) mediated necroptotic death pathways. These variations in cell death may be important for graft survival as necroptosis can lead to the release of chemotactic and activating danger molecules which have been shown to activate host immune cells. This pathway has yet to be studied in transplantation. We isolated and treated microvascular endothelial cells (MVECs) from C57BL/6 hearts with TNFα in the presence and absence of RIPK1 inhibitor, necrostatin-1 (nec-1), and pan-caspase inhibitor, zVAD-fmk to inhibit and induce necroptosis, respectively. Release of pro-inflammatory danger molecule HMGB1 was also measured in the supernatant of cells following treatment. In vivo heterotopic heart transplantation was also performed using wildtype C57BL/6 or C57BL/6-RIPK3-/-donors into fully MHC mismatched BALB/c mice following short term sirolimus treatment. Graft survival, viability and danger molecule release were determined at several timepoints. Our data shows that sirolimus treatment (9 days) markedly prolongs cardiac allograft survival of RIPK3-/- donor grafts compared with wildtype donor heart grafts into Balb/c recipients (95 + 5.8 vs 24 + 2.6 days p<0.001). In vitro, MVEC cell death is reduced by the RIPK1/RIPK3 inhibiting small molecule nec-1 in the presence of zVAD-fmk following TNFα treatment (25.9 + 2.73% vs 15.6 + 2%, PI positive at 48 hours, n=3, p<0.05). As well, necrosis and release of the pro-inflammatory danger molecule HMGB1 are attenuated in vivo in RIPK3 null heart allografts and in vitro with VEC after RIPK1/RIPK3 inhibition. Finally, quantitative blinded scoring of graft infiltration, necrotic cell death and endothelial damage were attenuated in RIP3 null hearts compared with wildtype allografts. These data suggest that RIPK1/RIPK3 contributes to inflammatory injury in cardiac allografts through MVEC necroptotic death and the release of danger molecules. The ability of immunosuppression to provide rejection protection or permit tolerance is influenced by the level of cell death and inflammation. We suggest that targeting RIPK1 and/or RIPK3 may be an important therapeutic strategy in solid organ transplantation.

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 score0.007

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 integrity0.0000.001
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 head0.004
GPT teacher head0.201
Teacher spread0.196 · 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".

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Citations0
Published2014
Admission routes1
Has abstractyes

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