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10.1016/j.actbio.2014.03.011 http://scihub22266oqcxt.onion/10.1016/j.actbio.2014.03.011 C4071604!4071604 !24657674     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24657674 &cmd=llinks): Failed to open stream: HTTP request failed! 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Alternative strategies to manipulate fibrocyte involvement in the fibrotic tissue response: pharmacokinetic inhibition and the feasibility of directed-adipogenic differentiation |pdf=|usr=}}{{24657674 }} gab.com Text Alternative strategies to manipulate fibrocyte involvement in the fibrotic tissue response: pharmacokinetic inhibition and the feasibility of directed-adipogenic differentiation JO: Acta Biomater http://www.kidney.de/pget.php?&tw=1&pmid=24657674 #FOAvip Fibrocytes have previously been identified as important mediators in several inflammatory and fibrotic diseases. However, there is no effective treatment thus far to reduce fibrotic tissue responses without affecting wound healing reactions. Here we investigate two strategies to alleviate fibrocyte interactions at the biomaterial interface, reducing collagen production and scar tissue formation. First, in an indirect approach, TGF-? inhibitor-SB431542 and IL-1?/TNF-? inhibitor SB203580 were locally released from scaffold implants to block their respective signaling pathways. We show that the inhibition of IL-1?/TNF-? has no influence on overall fibrotic tissue reactions to the implants. However, the reduction of localized TGF-? significantly decreases the fibrocyte accumulation and myofibroblast activation while reducing the fibrotic tissue formation. Since fibrocytes can be differentiated into non-fibrotic cell types, such as adipocytes, we further sought a more direct approach to reduce fibrocyte responses by directing fibrocyte differentiation into adipocytes. Interestingly, by initiating fibrocyte-to-adipocyte differentiation through sustained differentiation cocktail release, we find that adipogenic differentiation forces incoming fibrocytes away from the traditional myofibroblast lineage, leading to a substantial reduction in the collagen formation and fibrotic response. Our results support a novel and effective strategy to improve implant safety by reducing implant-associated fibrotic tissue reactions via directing non-fibrotic differentiation of fibrocytes. Twit Text FOAVip Alternative strategies to manipulate fibrocyte involvement in the fibrotic tissue response: pharmacokinetic inhibition and the feasibility of directed-adipogenic differentiation ????Acta Biomater http://www.kidney.de/pget.php?&tw=1&pmid=24657674 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24657674 #FOAvip English Wikipedia <ref>{{Cite pmid|24657674 }}</ref> Alternative strategies to manipulate fibrocyte involvement in the fibrotic tissue response: pharmacokinetic inhibition and the feasibility of directed-adipogenic differentiation #MMPMID24657674 Baker DW ; Tsai YT ; Weng H ; Tang L Acta Biomater 2014[Jul]; 10 (7 ): 3108-16 PMID24657674 show ga Fibrocytes have previously been identified as important mediators in several inflammatory and fibrotic diseases. However, there is no effective treatment thus far to reduce fibrotic tissue responses without affecting wound healing reactions. Here we investigate two strategies to alleviate fibrocyte interactions at the biomaterial interface, reducing collagen production and scar tissue formation. First, in an indirect approach, TGF-? inhibitor-SB431542 and IL-1?/TNF-? inhibitor SB203580 were locally released from scaffold implants to block their respective signaling pathways. We show that the inhibition of IL-1?/TNF-? has no influence on overall fibrotic tissue reactions to the implants. However, the reduction of localized TGF-? significantly decreases the fibrocyte accumulation and myofibroblast activation while reducing the fibrotic tissue formation. Since fibrocytes can be differentiated into non-fibrotic cell types, such as adipocytes, we further sought a more direct approach to reduce fibrocyte responses by directing fibrocyte differentiation into adipocytes. Interestingly, by initiating fibrocyte-to-adipocyte differentiation through sustained differentiation cocktail release, we find that adipogenic differentiation forces incoming fibrocytes away from the traditional myofibroblast lineage, leading to a substantial reduction in the collagen formation and fibrotic response. Our results support a novel and effective strategy to improve implant safety by reducing implant-associated fibrotic tissue reactions via directing non-fibrotic differentiation of fibrocytes. |*Cell Differentiation [MESH] |*Pharmacokinetics [MESH] |Adipose Tissue/*cytology/drug effects [MESH] |Animals [MESH] |Benzamides/pharmacology [MESH] |Dioxoles/pharmacology [MESH] |Feasibility Studies [MESH] |Fibroblasts/cytology [MESH] |Fibrosis [MESH] |Mice [MESH] |Mice, Inbred BALB C [MESH]Alternative strategies to manipulate fibrocyte involvement in the fibr(epmc).pdf DeepDyve Pubget Overpricing