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10.1016/j.stemcr.2016.05.002 http://scihub22266oqcxt.onion/10.1016/j.stemcr.2016.05.002 C4911503!4911503 !27264973     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27264973 &cmd=llinks): Failed to open stream: HTTP request failed! 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Sepsis Induces Hematopoietic Stem Cell Exhaustion and Myelosuppression through Distinct Contributions of TRIF and MYD88 |pdf=|usr=}}{{27264973 }} gab.com Text Sepsis Induces Hematopoietic Stem Cell Exhaustion and Myelosuppression through Distinct Contributions of TRIF and MYD88 JO: Stem Cell Reports http://www.kidney.de/pget.php?&tw=1&pmid=27264973 #FOAvip Toll-like receptor 4 (TLR4) plays a central role in host responses to bacterial infection, but the precise mechanism(s) by which its downstream signaling components coordinate the bone marrow response to sepsis is poorly understood. Using mice deficient in TLR4 downstream adapters MYD88 or TRIF, we demonstrate that both cell-autonomous and non-cell-autonomous MYD88 activation are major causes of myelosuppression during sepsis, while having a modest impact on hematopoietic stem cell (HSC) functions. In contrast, cell-intrinsic TRIF activation severely compromises HSC self-renewal without directly affecting myeloid cells. Lipopolysaccharide-induced activation of MYD88 or TRIF contributes to cell-cycle activation of HSC and induces rapid and permanent changes in transcriptional programs, as indicated by persistent downregulation of Spi1 and CebpA expression after transplantation. Thus, distinct mechanisms downstream of TLR4 signaling mediate myelosuppression and HSC exhaustion during sepsis through unique effects of MyD88 and TRIF. Twit Text FOAVip Sepsis Induces Hematopoietic Stem Cell Exhaustion and Myelosuppression through Distinct Contributions of TRIF and MYD88 ????Stem Cell Reports http://www.kidney.de/pget.php?&tw=1&pmid=27264973 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27264973 #FOAvip English Wikipedia <ref>{{Cite pmid|27264973 }}</ref> Sepsis Induces Hematopoietic Stem Cell Exhaustion and Myelosuppression through Distinct Contributions of TRIF and MYD88 #MMPMID27264973 Zhang H ; Rodriguez S ; Wang L ; Wang S ; Serezani H ; Kapur R ; Cardoso AA ; Carlesso N Stem Cell Reports 2016[Jun]; 6 (6 ): 940-956 PMID27264973 show ga Toll-like receptor 4 (TLR4) plays a central role in host responses to bacterial infection, but the precise mechanism(s) by which its downstream signaling components coordinate the bone marrow response to sepsis is poorly understood. Using mice deficient in TLR4 downstream adapters MYD88 or TRIF, we demonstrate that both cell-autonomous and non-cell-autonomous MYD88 activation are major causes of myelosuppression during sepsis, while having a modest impact on hematopoietic stem cell (HSC) functions. In contrast, cell-intrinsic TRIF activation severely compromises HSC self-renewal without directly affecting myeloid cells. Lipopolysaccharide-induced activation of MYD88 or TRIF contributes to cell-cycle activation of HSC and induces rapid and permanent changes in transcriptional programs, as indicated by persistent downregulation of Spi1 and CebpA expression after transplantation. Thus, distinct mechanisms downstream of TLR4 signaling mediate myelosuppression and HSC exhaustion during sepsis through unique effects of MyD88 and TRIF. |Adaptor Proteins, Vesicular Transport/deficiency/genetics/*immunology [MESH] |Animals [MESH] |CCAAT-Enhancer-Binding Proteins/genetics/immunology [MESH] |Cell Cycle [MESH] |Disease Models, Animal [MESH] |Gene Expression Regulation [MESH] |Hematopoietic Stem Cells/immunology/*pathology [MESH] |Lipopolysaccharides [MESH] |Mice [MESH] |Mice, Knockout [MESH] |Myeloid Cells/immunology/*pathology [MESH] |Myeloid Differentiation Factor 88/deficiency/genetics/*immunology [MESH] |Proto-Oncogene Proteins/genetics/immunology [MESH] |Sepsis/genetics/*immunology/pathology [MESH] |Signal Transduction [MESH] |Toll-Like Receptor 4/genetics/immunology [MESH] |Trans-Activators/genetics/immunology [MESH]Sepsis Induces Hematopoietic Stem Cell Exhaustion and Myelosuppression(epmc).pdf DeepDyve Pubget Overpricing