| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 8437399 | EBioMedicine | 2018 | 12 Pages |
Abstract
Alternative (M2-type) macrophage activation through IL-4Rα promotes liver inflammation and fibrosis progression but speeds up fibrosis reversal. This demonstrates context dependent, opposing roles of M2-type macrophages. During reversal IL-4Rα induces fibrolytic MMPs, especially MMP-12, through STAT6. Liver-specific antisense oligonucleotides efficiently block IL-4Rα expression and attenuate fibrosis progression.
Keywords
ECMARG1DKOPDGFDAPIHYPCCl4iNOSASOIFNγGAPDHqPCRTGFβ1CCL2Mrc1α-SMAHSCMMP12MMPIL-4RαCOL1A14,6-diamidino-2-phenylindoleantisense oligonucleotidearginase 1interferon-gammatumor necrosis factor alphastandard error of the meanTIMPHepatic stellate cellinducible nitric oxide synthaseTNF-αFibrosisExtracellular matrixmatrix metalloproteinaseMacrophageSEMTissue inhibitor of metalloproteinase 1double knockoutwildtypehydroxyprolineReversalquantitative polymerase chain reactionbody weightProgressionLiverCarbon tetrachloridechemokine (C-C motif) ligand 2glyceraldehyde 3-phosphate dehydrogenase
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Authors
Shih-Yen Weng, Xiaoyu Wang, Santosh Vijayan, Yilang Tang, Yong Ook Kim, Kornelius Padberg, Tommy Regen, Olena Molokanova, Tao Chen, Tobias Bopp, Hansjörg Schild, Frank Brombacher, Jeff R. Crosby, Michael L. McCaleb, Ari Waisman, Ernesto Bockamp,