FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2891515530> ?p ?o ?g. }

• W2891515530 endingPage "2072" @default.
• W2891515530 startingPage "2060" @default.
• W2891515530 abstract "Hepatic ischemia-reperfusion (I/R) injury, which is mainly induced by inflammation and unstable intracellular ions, is a major negative consequence of surgery that compromises hepatic function. However, the exact mechanisms of liver I/R injury have not been determined. Positive crosstalk with the Ca2+/CaMKII pathway is required for complete activation of the TLR4 pathway and inflammation. We previously found that miR-148a, which decreased in abundance with increasing reperfusion time, targeted and repressed the expression of CaMKIIα. In the present study, we examined the role of the miR-148a machinery in I/R-induced Ca2+/CaMKII and TLR4 signaling changes, inflammation, and liver dysfunction in vivo and in vitro.Liver function was evaluated by serum aminotransferase levels and hematoxylin-eosin (HE) staining. Inflammatory factors were detected by enzyme-linked immunosorbent assay. Gene and protein expression were assessed by RT-PCR and western blot. Small interfering RNA was used to silence target gene expression. HE staining and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling were used to measure hepatic tissue apoptosis. These assays were performed to identify factors upregulated in hepatic I/R injury and downregulated by miR-148a.We manifested that expression of CaMKIIα and phosphorylation of TAK1 and IRF3 were elevated in hypoxia/reoxygenation (H/R)-treated primary Kupffer cells (KCs) and liver tissue of I/R-treated mice, but these effects were attenuated by treatment with miR-148a mimic and were accompanied by the alleviation of liver dysfunction and hepatocellular apoptosis. Luciferase reporter experiments showed that miR148a suppressed luciferase activity by almost 60%. Moreover, knockdown of CaMKIIα in H/R KCs led to significant deficiencies in p-TAK1, P-IRF3, IL-6, and TNF-α, which was consistent with the effects of miR-148a overexpression. Otherwise, the same trend of activation of TAK1 and IRF3 and inflammatory factors in vitro was observed in the siTAK1 + siIRF3 group compared with the siCaMKIIα group.Taken together, we conclude that miR-148a may mitigate hepatic I/R injury by ameliorating TLR4-mediated inflammation via targeting CaMKIIα in vitro and in vivo." @default.
• W2891515530 created "2018-09-27" @default.
• W2891515530 creator A5001401611 @default.
• W2891515530 creator A5007050514 @default.
• W2891515530 creator A5029082179 @default.
• W2891515530 creator A5044479302 @default.
• W2891515530 creator A5050403219 @default.
• W2891515530 creator A5076649173 @default.
• W2891515530 creator A5081675173 @default.
• W2891515530 creator A5091598293 @default.
• W2891515530 date "2018-01-01" @default.
• W2891515530 modified "2023-09-29" @default.
• W2891515530 title "Role of miR-148a in Mitigating Hepatic Ischemia-Reperfusion Injury by Repressing the TLR4 Signaling Pathway via Targeting CaMKIIα in Vivo and in Vitro" @default.
• W2891515530 cites W120883508 @default.
• W2891515530 cites W1261642005 @default.
• W2891515530 cites W1489742081 @default.
• W2891515530 cites W1574235863 @default.
• W2891515530 cites W1578909391 @default.
• W2891515530 cites W162447880 @default.
• W2891515530 cites W1906591077 @default.
• W2891515530 cites W1974408946 @default.
• W2891515530 cites W1978910929 @default.
• W2891515530 cites W1979601962 @default.
• W2891515530 cites W1998404710 @default.
• W2891515530 cites W2017583361 @default.
• W2891515530 cites W2018062403 @default.
• W2891515530 cites W2036941062 @default.
• W2891515530 cites W2039118309 @default.
• W2891515530 cites W2041651305 @default.
• W2891515530 cites W2045641591 @default.
• W2891515530 cites W2054543879 @default.
• W2891515530 cites W2057758077 @default.
• W2891515530 cites W2059427568 @default.
• W2891515530 cites W2077291760 @default.
• W2891515530 cites W2079113729 @default.
• W2891515530 cites W2080204426 @default.
• W2891515530 cites W2088302893 @default.
• W2891515530 cites W2088931568 @default.
• W2891515530 cites W2098015915 @default.
• W2891515530 cites W2107277218 @default.
• W2891515530 cites W2115734680 @default.
• W2891515530 cites W2118998161 @default.
• W2891515530 cites W2167875873 @default.
• W2891515530 cites W2341631555 @default.
• W2891515530 cites W2371948111 @default.
• W2891515530 cites W2412815278 @default.
• W2891515530 cites W2518860062 @default.
• W2891515530 doi "https://doi.org/10.1159/000493716" @default.
• W2891515530 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30244246" @default.
• W2891515530 hasPublicationYear "2018" @default.
• W2891515530 type Work @default.
• W2891515530 sameAs 2891515530 @default.
• W2891515530 citedByCount "28" @default.
• W2891515530 countsByYear W28915155302019 @default.
• W2891515530 countsByYear W28915155302020 @default.
• W2891515530 countsByYear W28915155302021 @default.
• W2891515530 countsByYear W28915155302022 @default.
• W2891515530 countsByYear W28915155302023 @default.
• W2891515530 crossrefType "journal-article" @default.
• W2891515530 hasAuthorship W2891515530A5001401611 @default.
• W2891515530 hasAuthorship W2891515530A5007050514 @default.
• W2891515530 hasAuthorship W2891515530A5029082179 @default.
• W2891515530 hasAuthorship W2891515530A5044479302 @default.
• W2891515530 hasAuthorship W2891515530A5050403219 @default.
• W2891515530 hasAuthorship W2891515530A5076649173 @default.
• W2891515530 hasAuthorship W2891515530A5081675173 @default.
• W2891515530 hasAuthorship W2891515530A5091598293 @default.
• W2891515530 hasBestOaLocation W28915155301 @default.
• W2891515530 hasConcept C104317684 @default.
• W2891515530 hasConcept C126322002 @default.
• W2891515530 hasConcept C127561419 @default.
• W2891515530 hasConcept C134018914 @default.
• W2891515530 hasConcept C150903083 @default.
• W2891515530 hasConcept C153911025 @default.
• W2891515530 hasConcept C185592680 @default.
• W2891515530 hasConcept C190283241 @default.
• W2891515530 hasConcept C203014093 @default.
• W2891515530 hasConcept C207001950 @default.
• W2891515530 hasConcept C22615655 @default.
• W2891515530 hasConcept C2776070231 @default.
• W2891515530 hasConcept C2776415932 @default.
• W2891515530 hasConcept C2776637226 @default.
• W2891515530 hasConcept C2776914184 @default.
• W2891515530 hasConcept C2780114680 @default.
• W2891515530 hasConcept C54009773 @default.
• W2891515530 hasConcept C541997718 @default.
• W2891515530 hasConcept C55493867 @default.
• W2891515530 hasConcept C62478195 @default.
• W2891515530 hasConcept C71924100 @default.
• W2891515530 hasConcept C86803240 @default.
• W2891515530 hasConcept C95444343 @default.
• W2891515530 hasConceptScore W2891515530C104317684 @default.
• W2891515530 hasConceptScore W2891515530C126322002 @default.
• W2891515530 hasConceptScore W2891515530C127561419 @default.
• W2891515530 hasConceptScore W2891515530C134018914 @default.
• W2891515530 hasConceptScore W2891515530C150903083 @default.
• W2891515530 hasConceptScore W2891515530C153911025 @default.
• W2891515530 hasConceptScore W2891515530C185592680 @default.

• next