FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2484877107> ?p ?o ?g. }

• W2484877107 endingPage "e0159724" @default.
• W2484877107 startingPage "e0159724" @default.
• W2484877107 abstract "Inflammatory M1 spectrum macrophages protect from infection but can cause inflammatory disease and tissue damage, whereas alternatively activated/M2 spectrum macrophages reduce inflammation and promote tissue repair. Modulation of macrophage phenotype may be therapeutically beneficial and requires further understanding of the molecular programs that control macrophage differentiation. A potential mechanism by which macrophages differentiate may be through microRNA (miRNA), which bind to messenger RNA and post-transcriptionally modify gene expression, cell phenotype and function. We hypothesized that the inflammation-associated miRNA, miR-155, would be required for typical development of macrophage inflammatory state. miR-155 was rapidly up-regulated over 100-fold in inflammatory M1(LPS + IFN-γ), but not M2(IL-4), macrophages. Inflammatory genes Inos, Il1b and Tnfa and their corresponding protein or enzymatic products were reduced up to 72% in miR-155 knockout mouse M1(LPS + IFN-γ) macrophages, but miR-155 deficiency did not affect expression of the M2-associated gene Arg1 in M2(IL-4) macrophages. Additionally, a miR-155 oligonucleotide inhibitor efficiently suppressed Inos and Tnfa gene expression in wild-type M1(LPS + IFN-γ) macrophages. Comparative transcriptional profiling of unstimulated and M1(LPS + IFN-γ) macrophages derived from wild-type (WT) and miR-155 knockout (KO) mice revealed that half (approximately 650 genes) of the signature we previously identified in WT M1(LPS + IFN-γ) macrophages was dependent on miR-155. Real-Time PCR of independent datasets confirmed that miR-155 contributed to suppression of its validated mRNA targets Inpp5d, Tspan14, Ptprj and Mafb and induction of Inos, Il1b, Tnfa, Il6 and Il12. Overall, these data indicate that miR-155 plays an essential role in driving the inflammatory phenotype of M1(LPS+ IFN-γ) macrophages." @default.
• W2484877107 created "2016-08-23" @default.
• W2484877107 creator A5012696999 @default.
• W2484877107 creator A5019580678 @default.
• W2484877107 creator A5051353828 @default.
• W2484877107 creator A5071211166 @default.
• W2484877107 creator A5090283584 @default.
• W2484877107 date "2016-07-22" @default.
• W2484877107 modified "2023-10-17" @default.
• W2484877107 title "Control of the Inflammatory Macrophage Transcriptional Signature by miR-155" @default.
• W2484877107 cites W144423133 @default.
• W2484877107 cites W1506057870 @default.
• W2484877107 cites W1664596139 @default.
• W2484877107 cites W1797422316 @default.
• W2484877107 cites W1858233563 @default.
• W2484877107 cites W1923917571 @default.
• W2484877107 cites W1962869168 @default.
• W2484877107 cites W196395934 @default.
• W2484877107 cites W1965345750 @default.
• W2484877107 cites W1974102799 @default.
• W2484877107 cites W1977859620 @default.
• W2484877107 cites W1981056356 @default.
• W2484877107 cites W1986342542 @default.
• W2484877107 cites W2002869490 @default.
• W2484877107 cites W2004428166 @default.
• W2484877107 cites W2012461622 @default.
• W2484877107 cites W2014869583 @default.
• W2484877107 cites W2014946489 @default.
• W2484877107 cites W2024704386 @default.
• W2484877107 cites W2038180405 @default.
• W2484877107 cites W2038689279 @default.
• W2484877107 cites W2041363468 @default.
• W2484877107 cites W2042629891 @default.
• W2484877107 cites W2046635810 @default.
• W2484877107 cites W2049772720 @default.
• W2484877107 cites W2050091174 @default.
• W2484877107 cites W2054472394 @default.
• W2484877107 cites W2061123122 @default.
• W2484877107 cites W2063080163 @default.
• W2484877107 cites W2070855360 @default.
• W2484877107 cites W2077124851 @default.
• W2484877107 cites W2082678538 @default.
• W2484877107 cites W2094524631 @default.
• W2484877107 cites W2094659815 @default.
• W2484877107 cites W2099350622 @default.
• W2484877107 cites W2102468603 @default.
• W2484877107 cites W2103018087 @default.
• W2484877107 cites W2103392842 @default.
• W2484877107 cites W2103412440 @default.
• W2484877107 cites W2105156168 @default.
• W2484877107 cites W2107277218 @default.
• W2484877107 cites W2112828311 @default.
• W2484877107 cites W2113546559 @default.
• W2484877107 cites W2119656827 @default.
• W2484877107 cites W2124744205 @default.
• W2484877107 cites W2124756133 @default.
• W2484877107 cites W2128627731 @default.
• W2484877107 cites W2132281111 @default.
• W2484877107 cites W2134729461 @default.
• W2484877107 cites W2136188258 @default.
• W2484877107 cites W2140380746 @default.
• W2484877107 cites W2143216993 @default.
• W2484877107 cites W2143308901 @default.
• W2484877107 cites W2146358032 @default.
• W2484877107 cites W2155984519 @default.
• W2484877107 cites W2156023352 @default.
• W2484877107 cites W2159560463 @default.
• W2484877107 cites W2161456562 @default.
• W2484877107 cites W2162166699 @default.
• W2484877107 cites W2162762911 @default.
• W2484877107 cites W2167830630 @default.
• W2484877107 cites W2169704861 @default.
• W2484877107 cites W2171028311 @default.
• W2484877107 cites W2192080449 @default.
• W2484877107 cites W2204020009 @default.
• W2484877107 cites W2209250550 @default.
• W2484877107 cites W2220734173 @default.
• W2484877107 cites W2234441800 @default.
• W2484877107 cites W2260460109 @default.
• W2484877107 cites W4230963859 @default.
• W2484877107 cites W4245806510 @default.
• W2484877107 doi "https://doi.org/10.1371/journal.pone.0159724" @default.
• W2484877107 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4957803" @default.
• W2484877107 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/27447824" @default.
• W2484877107 hasPublicationYear "2016" @default.
• W2484877107 type Work @default.
• W2484877107 sameAs 2484877107 @default.
• W2484877107 citedByCount "112" @default.
• W2484877107 countsByYear W24848771072016 @default.
• W2484877107 countsByYear W24848771072017 @default.
• W2484877107 countsByYear W24848771072018 @default.
• W2484877107 countsByYear W24848771072019 @default.
• W2484877107 countsByYear W24848771072020 @default.
• W2484877107 countsByYear W24848771072021 @default.
• W2484877107 countsByYear W24848771072022 @default.
• W2484877107 countsByYear W24848771072023 @default.
• W2484877107 crossrefType "journal-article" @default.
• W2484877107 hasAuthorship W2484877107A5012696999 @default.

• next