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dc.contributor.authorKelly, John L
dc.contributor.authorFindlay, Michael W
dc.contributor.authorKnight, Kenneth R
dc.contributor.authorPenington, Anthony
dc.contributor.authorThompson, Erik W
dc.contributor.authorMessina, Aurora
dc.contributor.authorMorrison, Wayne A
dc.date.accessioned2011-10-03T14:18:50Z
dc.date.available2011-10-03T14:18:50Z
dc.date.issued2006-07
dc.identifier.citationContact with existing adipose tissue is inductive for adipogenesis in matrigel. 2006, 12 (7):2041-7 Tissue Eng.en
dc.identifier.issn1076-3279
dc.identifier.pmid16889532
dc.identifier.doi10.1089/ten.2006.12.2041
dc.identifier.urihttp://hdl.handle.net/10147/143785
dc.descriptionThe effect of adipose tissue on inductive adipogenesis within Matrigel (BD Biosciences) was assessed by using a murine chamber model containing a vascular pedicle. Three-chamber configurations that varied in the access to an adipose tissue source were used, including sealed- and open-chamber groups that had no access and limited access, respectively, to the surrounding adipose tissue, and a sealed-chamber group in which adipose tissue was placed as an autograft. All groups showed neovascularization, but varied in the amount of adipogenesis seen in direct relation to their access to preexisting adipose tissue: open chambers showed strong adipogenesis, whereas the sealed chambers had little or no adipose tissue; adipogenesis was restored in the autograft chamber group that contained 2- to 5-mg fat autografts. These showed significantly more adipogenesis than the sealed chambers with no autograft ( p < 0.01). Autografts with 1mg of fat were capable of producing adipogenesis but did so less consistently than the larger autografts. These findings have important implications for adipose tissue engineering strategies and for understanding de novo production of adipose tissue.en
dc.description.abstractThe effect of adipose tissue on inductive adipogenesis within Matrigel (BD Biosciences) was assessed by using a murine chamber model containing a vascular pedicle. Three-chamber configurations that varied in the access to an adipose tissue source were used, including sealed- and open-chamber groups that had no access and limited access, respectively, to the surrounding adipose tissue, and a sealed-chamber group in which adipose tissue was placed as an autograft. All groups showed neovascularization, but varied in the amount of adipogenesis seen in direct relation to their access to preexisting adipose tissue: open chambers showed strong adipogenesis, whereas the sealed chambers had little or no adipose tissue; adipogenesis was restored in the autograft chamber group that contained 2- to 5-mg fat autografts. These showed significantly more adipogenesis than the sealed chambers with no autograft ( p < 0.01). Autografts with 1mg of fat were capable of producing adipogenesis but did so less consistently than the larger autografts. These findings have important implications for adipose tissue engineering strategies and for understanding de novo production of adipose tissue.
dc.language.isoenen
dc.publisherMary Ann Liebert Incen
dc.relation.urlhttp://www.liebertonline.com/doi/abs/10.1089/ten.2006.12.2041en
dc.subject.meshAdipogenesis
dc.subject.meshAdipose Tissue
dc.subject.meshAnimals
dc.subject.meshBiocompatible Materials
dc.subject.meshCell Communication
dc.subject.meshCell Differentiation
dc.subject.meshCollagen
dc.subject.meshDrug Combinations
dc.subject.meshLaminin
dc.subject.meshMice
dc.subject.meshNeovascularization, Physiologic
dc.subject.meshProteoglycans
dc.subject.meshTransplantation, Autologous
dc.titleContact with existing adipose tissue is inductive for adipogenesis in matrigel.en
dc.typeArticleen
dc.contributor.departmentBernard O'Brien Institute of Microsurgery, Melbourne, Australia.en
dc.identifier.journalTissue engineeringen
dc.description.provinceConnacht
html.description.abstractThe effect of adipose tissue on inductive adipogenesis within Matrigel (BD Biosciences) was assessed by using a murine chamber model containing a vascular pedicle. Three-chamber configurations that varied in the access to an adipose tissue source were used, including sealed- and open-chamber groups that had no access and limited access, respectively, to the surrounding adipose tissue, and a sealed-chamber group in which adipose tissue was placed as an autograft. All groups showed neovascularization, but varied in the amount of adipogenesis seen in direct relation to their access to preexisting adipose tissue: open chambers showed strong adipogenesis, whereas the sealed chambers had little or no adipose tissue; adipogenesis was restored in the autograft chamber group that contained 2- to 5-mg fat autografts. These showed significantly more adipogenesis than the sealed chambers with no autograft ( p < 0.01). Autografts with 1mg of fat were capable of producing adipogenesis but did so less consistently than the larger autografts. These findings have important implications for adipose tissue engineering strategies and for understanding de novo production of adipose tissue.


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