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10.1371/journal.pone.0179257 http://scihub22266oqcxt.onion/10.1371/journal.pone.0179257 C5466303!5466303 !28598999     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28598999 &cmd=llinks): Failed to open stream: HTTP request failed! 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Lymphatic endothelial progenitors originate from plastic myeloid cells activated by toll-like receptor-4 |pdf=|usr=}}{{28598999 }} gab.com Text Lymphatic endothelial progenitors originate from plastic myeloid cells activated by toll-like receptor-4 JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=28598999 #FOAvip BACKGROUND: Myeloid-derived lymphatic endothelial cells (M-LECP) are induced by inflammation and play an important role in adult lymphangiogenesis. However, the mechanisms driving M-LECP differentiation are currently unclear. We previously showed that activation of Toll-like receptor-4 (TLR4) induces myeloid-lymphatic transition (MLT) of immortalized mouse myeloid cells. Here the goals were to assess the potential of different TLR4 ligands to induce pro-lymphatic reprogramming in human and mouse primary myeloid cells and to identify transcriptional changes regulating this process. METHODOLOGY/PRINCIPAL FINDINGS: Human and mouse myeloid cells were reprogrammed to the lymphatic phenotype by TLR4 ligands including lipopolysaccharide (LPS), recombinant high mobility group box 1 protein (HMGB1), and paclitaxel. TLR4 induced similar MLT in cells from mice of different strains and immune status. Commonly induced genes were detected by transcriptional profiling in human and mouse myeloid cells from either immunocompetent or immunodeficient mice. Shared trends included: (1) novel expression of lymphatic-specific markers vascular endothelial growth factor receptor-3 (VEGFR-3), lymphatic vessel endothelial hyaluronan receptor-1 (LYVE-1) and podoplanin (PDPN) largely absent prior to induction; (2) lack of notable changes in blood vessel-specific markers; (3) transient expression of VEGFR-3, but sustained increase of vascular endothelial growth factor-C (VEGF-C) and a variety of inflammatory cytokines; (4) dependency of VEGFR-3 upregulation and other LEC genes on NF-?B; and (5) novel expression of lymphatic-specific (e.g., PROX1) and stem/progenitor (e.g., E2F1) transcription factors known for their roles in adult and embryonic vascular formation. M-LECP generated by TLR4 ligands in vitro were functional in vivo as demonstrated by significantly increased lymphatic vessel density and lymphatic metastasis detected in orthotopic breast cancer models. CONCLUSIONS/SIGNIFICANCE: We established a novel TLR4-dependent protocol for in vitro production of functionally competent M-LECP from primary human or mouse myeloid cells and identified many potential regulators of this process. This information can be further exploited for research and therapeutic purposes. Twit Text FOAVip Lymphatic endothelial progenitors originate from plastic myeloid cells activated by toll-like receptor-4 ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=28598999 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28598999 #FOAvip English Wikipedia <ref>{{Cite pmid|28598999 }}</ref> Lymphatic endothelial progenitors originate from plastic myeloid cells activated by toll-like receptor-4 #MMPMID28598999 Volk-Draper LD ; Hall KL ; Wilber AC ; Ran S PLoS One 2017[]; 12 (6 ): e0179257 PMID28598999 show ga BACKGROUND: Myeloid-derived lymphatic endothelial cells (M-LECP) are induced by inflammation and play an important role in adult lymphangiogenesis. However, the mechanisms driving M-LECP differentiation are currently unclear. We previously showed that activation of Toll-like receptor-4 (TLR4) induces myeloid-lymphatic transition (MLT) of immortalized mouse myeloid cells. Here the goals were to assess the potential of different TLR4 ligands to induce pro-lymphatic reprogramming in human and mouse primary myeloid cells and to identify transcriptional changes regulating this process. METHODOLOGY/PRINCIPAL FINDINGS: Human and mouse myeloid cells were reprogrammed to the lymphatic phenotype by TLR4 ligands including lipopolysaccharide (LPS), recombinant high mobility group box 1 protein (HMGB1), and paclitaxel. TLR4 induced similar MLT in cells from mice of different strains and immune status. Commonly induced genes were detected by transcriptional profiling in human and mouse myeloid cells from either immunocompetent or immunodeficient mice. Shared trends included: (1) novel expression of lymphatic-specific markers vascular endothelial growth factor receptor-3 (VEGFR-3), lymphatic vessel endothelial hyaluronan receptor-1 (LYVE-1) and podoplanin (PDPN) largely absent prior to induction; (2) lack of notable changes in blood vessel-specific markers; (3) transient expression of VEGFR-3, but sustained increase of vascular endothelial growth factor-C (VEGF-C) and a variety of inflammatory cytokines; (4) dependency of VEGFR-3 upregulation and other LEC genes on NF-?B; and (5) novel expression of lymphatic-specific (e.g., PROX1) and stem/progenitor (e.g., E2F1) transcription factors known for their roles in adult and embryonic vascular formation. M-LECP generated by TLR4 ligands in vitro were functional in vivo as demonstrated by significantly increased lymphatic vessel density and lymphatic metastasis detected in orthotopic breast cancer models. CONCLUSIONS/SIGNIFICANCE: We established a novel TLR4-dependent protocol for in vitro production of functionally competent M-LECP from primary human or mouse myeloid cells and identified many potential regulators of this process. This information can be further exploited for research and therapeutic purposes. |*Cell Differentiation [MESH] |Animals [MESH] |Biomarkers [MESH] |CD11b Antigen/metabolism [MESH] |Disease Models, Animal [MESH] |Endothelial Cells/*cytology/*metabolism [MESH] |Female [MESH] |Gene Expression Regulation [MESH] |Heterografts [MESH] |Humans [MESH] |Immunocompromised Host [MESH] |Inflammation Mediators/metabolism [MESH] |Lipopolysaccharide Receptors/metabolism [MESH] |Lymphangiogenesis [MESH] |Mice [MESH] |Monocytes/metabolism [MESH] |Myeloid Cells/*cytology/*metabolism [MESH] |Neoplasm Metastasis [MESH] |Neoplasms/genetics/immunology/metabolism/pathology [MESH] |Phenotype [MESH] |Stem Cells/*cytology/*metabolism [MESH]Lymphatic endothelial progenitors originate from plastic myeloid cells(epmc).pdf DeepDyve Pubget Overpricing