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Interactive Role of TLR4 and TLR2 in Cardiac Functions During Stressful Conditions

2017· article· en· W2904135173 on OpenAlexaffabout
Ashim K. Bagchi, Gauri Akolkar, Soma Barman, Prathapan Ayyappan, Xi Shan YANG, Pawan K. Singal

Bibliographic record

VenueThe FASEB Journal · 2017
Typearticle
Languageen
FieldImmunology and Microbiology
TopicImmune Response and Inflammation
Canadian institutionsUniversity of Manitoba
Fundersnot available
KeywordsTLR2TLR4Downregulation and upregulationTumor necrosis factor alphaReceptorFibrosisMedicineInterleukinInflammationKnockout mouseIschemiaApoptosisToll-like receptorEndocrinologyInternal medicineCytokineBiologyInnate immune system

Abstract

fetched live from OpenAlex

An appropriate balance between anti‐inflammatory interleukin‐10 (IL‐10) and pro‐inflammatory tumor necrosis factor‐α (TNF‐α) cytokines has been suggested for a normal functioning of the heart. It has been suggested that toll‐like receptor 4 (TLR4) promotes IL‐10‐mediated cardiac cell survival while another receptor, TLR2, from the same family is detrimental. We examined the interactive role of these two innate signaling molecules (TLR4 and TLR2) under stressful conditions including interleukin‐10 knockout (IL‐10−/−) mice, global ischemia/reperfusion (I/R) injury rat hearts and shRNA experimental models. Circulating and myocardial levels of TNF‐α as well as apoptosis and fibrosis were higher in IL‐10−/− hearts. Increase in TLR2 in IL‐10−/− hearts indicated its negative regulation by IL‐10. The ex‐vivo I/R also caused a marked upregulation of TLR2 and TNF‐α as well as apoptotic and fibrotic signals. However, 40 min reperfusion with IL‐10 in the I/R hearts, triggered an increase in TLR4 expression. Increase in interleukin‐1 receptor‐associated kinase‐M (IRAK‐M) and IRAK‐2 activity during I/R injury suggested their role in TLR2 signaling. Inhibition of TLR4 activity as a consequence of RNAi‐mediated suppression of myeloid differentiation gene 88 (MyD88) suggested a MyD88‐dependent activation of TLR4. Inclusion of IL‐10 during reperfusion, also significantly downregulated the expression of IRAK‐2, TRAIP and apoptotic signals, caspase 3 and Bax/Bclxl ratio. IL‐10 reduced the TNF‐α receptor‐associated increase in TRAIP/TRADD ‐induced apoptosis during ischemia injury which led to an increase in IL‐1β to mitigate TGF‐βRII‐mediated fibrosis. IL‐10 mitigation of these changes suggests that IL‐10 stimulation through TLR4 signaling, dissociates IRAK‐4 into IRAK‐1 instead of IRAK‐2 and may be an important therapeutic approach in restoring heart health from I/R injury. Support or Funding Information Supported by Canadian Institutes of Health Research and Research Manitoba.

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 integrity0.0000.000
Insufficient payload (model declined to judge)0.0020.000

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 head0.006
GPT teacher head0.237
Teacher spread0.231 · 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
Published2017
Admission routes2
Has abstractyes

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