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lüll TWEAK/Fn14 signaling is required for liver regeneration after partial hepatectomy in mice Karaca G; Swiderska-Syn M; Xie G; Syn WK; Kruger L; Machado MV; Garman K; Choi SS; Michelotti GA; Burkly LC; Ochoa B; Diehl AMPLoS One 2014[]; 9 (1): e83987BACKGROUND & AIMS: Pro-inflammatory cytokines are important for liver regeneration after partial hepatectomy (PH). Expression of Fibroblast growth factor-inducible 14 (Fn14), the receptor for TNF-like weak inducer of apoptosis (TWEAK), is induced rapidly after PH and remains elevated throughout the period of peak hepatocyte replication. The role of Fn14 in post-PH liver regeneration is uncertain because Fn14 is expressed by liver progenitors and TWEAK-Fn14 interactions stimulate progenitor growth, but replication of mature hepatocytes is thought to drive liver regeneration after PH. METHODS: To clarify the role of TWEAK-Fn14 after PH, we compared post-PH regenerative responses in wild type (WT) mice, Fn14 knockout (KO) mice, TWEAK KO mice, and WT mice treated with anti-TWEAK antibodies. RESULTS: In WT mice, rare Fn14(+) cells localized with other progenitor markers in peri-portal areas before PH. PH rapidly increased proliferation of Fn14(+) cells; hepatocytic cells that expressed Fn14 and other progenitor markers, such as Lgr5, progressively accumulated from 12-8 h post-PH and then declined to baseline by 96 h. When TWEAK/Fn14 signaling was disrupted, progenitor accumulation, induction of pro-regenerative cytokines, hepatocyte and cholangiocyte proliferation, and over-all survival were inhibited, while post-PH liver damage and bilirubin levels were increased. TWEAK stimulated proliferation and increased Lgr5 expression in cultured liver progenitors, but had no effect on either parameter in cultured primary hepatocytes. CONCLUSIONS: TWEAK-FN14 signaling is necessary for the healthy adult liver to regenerate normally after acute partial hepatectomy.|*Hepatectomy[MESH]|*Liver Regeneration/drug effects[MESH]|*Signal Transduction/drug effects[MESH]|Animals[MESH]|Antibodies/pharmacology[MESH]|Cell Proliferation/drug effects[MESH]|Cytokine TWEAK[MESH]|Epithelial Cells/cytology/drug effects[MESH]|Gene Deletion[MESH]|Hepatocytes/cytology/drug effects/metabolism[MESH]|Liver/cytology/*metabolism/*surgery[MESH]|Mice[MESH]|Mice, Inbred C57BL[MESH]|Mice, Knockout[MESH]|Mitogens/metabolism[MESH]|Receptors, Tumor Necrosis Factor/*metabolism[MESH]|TWEAK Receptor[MESH]|Tumor Necrosis Factor Inhibitors[MESH]|Tumor Necrosis Factors/*metabolism[MESH] |