The fibroblast‐populated collagen matrix as a model of wound healing: a review of the evidence

Carlson, Mark A.; Longaker, Michael T.

doi:10.1111/j.1067-1927.2004.012208.x

Cited by 158 publications

(154 citation statements)

References 161 publications

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“…43 The reorganizing ECM has been shown to affect the wound contraction. 38 To further elucidate the functional role of FGFR1OP2/wit3.0, we have developed fibroblastic cells that were derived from mouse ES cells carrying Floating collagen gel contraction assay revealed that both oral and skin fibroblasts transduced by FGFR1OP2/wit3.0␤ lentiviral vectors (dotted lines) increased gel contraction rates. E: SNP1, SNP2, and SNP1/2 of FGFR1OP2/wit3.0␤ increased collagen gel contraction rates.…”

Section: Discussionmentioning

confidence: 99%

Small Cytoskeleton-Associated Molecule, Fibroblast Growth Factor Receptor 1 Oncogene Partner 2/Wound Inducible Transcript-3.0 (FGFR1OP2/wit3.0), Facilitates Fibroblast-Driven Wound Closure

Lin

Hokugo

Choi

et al. 2010

The American Journal of Pathology

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Wounds created in the oral cavity heal rapidly and leave minimal scarring. We have examined a role of a previously isolated cDNA from oral wounds encoding wound inducible transcript-3.0 (wit3.0) , also known as fibroblast growth factor receptor 1 oncogene partner 2 (FGFR1OP2). FGFR1OP2/wit3.0 was highly expressed in oral wound fibroblasts without noticeable up-regulation of ␣-smooth muscle actin. In silico analyses , denaturing and nondenaturing gel Western blot , and immunocytology together demonstrated that FGFR1OP2/wit3.0 were able to dimerize and oligomerize through coiled-coil structures and appeared to associate with cytoskeleton networks in oral wound fibroblasts. Overexpression of FGFR1OP2/ wit3.0 increased the floating collagen gel contraction of naïve oral fibroblasts to the level of oral wound fibroblasts , which was in turn attenuated by smallinterfering RNA knockdown. The FGFR1OP2/wit3.0 synthesis did not affect the expression of collagen I as well as procontractile peptides such as ␣-smooth muscle actin , and transforming growth factor-␤1 had no effect on FGFR1OP2/wit3.0 expression. Fibroblastic cells derived from embryonic stem cells carrying FGFR1OP2/wit3.0 (؉/؊) mutation showed significant retardation in cell migration. Thus , we postulate that FGFR1OP2/wit3.0 may regulate cell motility and stimulate wound closure. FGFR1OP2/wit3.0 was not upregulated during skin wound healing; however , when treated with FGFR1OP2/wit3.0 -expression vector, the skin wound closure was significantly accelerated, resulting in the limited granulation tissue formation. Our data suggest that FGFR1OP2/wit3.0 may possess a therapeutic potential for wound management. (Am J

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Section: Discussionmentioning

confidence: 99%

Small Cytoskeleton-Associated Molecule, Fibroblast Growth Factor Receptor 1 Oncogene Partner 2/Wound Inducible Transcript-3.0 (FGFR1OP2/wit3.0), Facilitates Fibroblast-Driven Wound Closure

Lin

Hokugo

Choi

et al. 2010

The American Journal of Pathology

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“…52 Cocultured fibroblast would not cause any concern in terms of overproliferation since it was shown that fibroblasts in floating collagen matrices have low levels of DNA synthesis and become quiescent. [53][54][55] Thus, bystander fibroblasts will not have any negative impact on islet viability and function.…”

Section: Discussionmentioning

confidence: 99%

Mouse Pancreatic Islets Are Resistant to Indoleamine 2,3 Dioxygenase-Induced General Control Nonderepressible-2 Kinase Stress Pathway and Maintain Normal Viability and Function

Jalili

Forouzandeh

Moeenrezakhanlou

et al. 2009

The American Journal of Pathology

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Islet transplantation is a promising treatment for diabetes. However, it faces several challenges including requirement of systemic immunosuppression. Indoleamine 2,3-dioxygenase (IDO), a tryptophan degrading enzyme, is a potent immunomodulatory factor. Local expression of IDO in bystander fibroblasts suppresses islet allogeneic immune response in vitro. The aim of the present study was to investigate the impact of IDO on viability and function of mouse islets embedded within IDO-expressing fibroblastpopulated collagen scaffold. Mouse islets were embedded within collagen matrix populated with IDO adenovector-transduced or control fibroblasts. Proliferation, insulin content, glucose responsiveness, and activation of general control nonderepressible-2 kinase stress-responsive pathway were then measured in IDOexposed islets. In vivo viabilities of composite islet grafts were also tested in a syngeneic diabetic animal model. No reduction in islet cells proliferation was detected in both IDO-expressing and control composites compared to the baseline rates. Islet functional studies showed normal insulin content and secretion in both preparations. In contrast to lymphocytes, general control nonderepressible-2 kinase pathway was not activated in islets cocultured with IDO-expressing fibroblasts. When transplanted to diabetic mice, syngeneic IDO-expressing composite islet grafts were functional up to 100 days tested. These findings collectively confirm normal viability and functionality of islets cocultured with IDO-expressing cells and indicate the feasibility of development of a functional nonrejectable islet graft.

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“…Cells interacting with collagen matrices exhibit distinct patterns of signaling and migration [18][19][20][21] and remodel matrices both locally and globally [5,6,[22][23][24]] to achieve tensional homeostasis [25,26]. While cells on planar surfaces can modulate their cytoskeletal function in response to surface mechanics [27,28], they have little capacity to modulate the overall molecular organization and mechanical properties of the ECM-coated planar surface itself.…”

Section: The Four Quadrants Of Cell Mechanicsmentioning

confidence: 99%

Fibroblast mechanics in 3D collagen matrices☆

Rhee

Grinnell²

2007

Advanced Drug Delivery Reviews

166

115

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Connective tissues provide mechanical support and frameworks for the other tissues of the body. Type 1 collagen is the major protein component of ordinary connective tissue, and fibroblasts are the cell type primarily responsible for its biosynthesis and remodeling. Research on fibroblasts interacting with collagen matrices explores all four quadrants of cell mechanics: pro-migratory vs. pro-contractile growth factor environments on one axis; high tension vs. low tension cell-matrix interactions on the other. The dendritic fibroblast -probably equivalent to the resting tissue fibroblast -can be observed only in the low tension quadrant and generally has not been appreciated from research on cells incubated with planar culture surfaces. Fibroblasts in the low tension quadrant require microtubules for formation of dendritic extensions, whereas fibroblasts in the high tension quadrant require microtubules for polarization but not for spreading. Ruffling of dendritic extensions rather than their overall protrusion or retraction provides the mechanism for remodeling of floating collagen matrices, and floating matrix remodeling likely reflects a model of tissue mechanical homeostasis.

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The fibroblast‐populated collagen matrix as a model of wound healing: a review of the evidence

Cited by 158 publications

References 161 publications

Small Cytoskeleton-Associated Molecule, Fibroblast Growth Factor Receptor 1 Oncogene Partner 2/Wound Inducible Transcript-3.0 (FGFR1OP2/wit3.0), Facilitates Fibroblast-Driven Wound Closure

Small Cytoskeleton-Associated Molecule, Fibroblast Growth Factor Receptor 1 Oncogene Partner 2/Wound Inducible Transcript-3.0 (FGFR1OP2/wit3.0), Facilitates Fibroblast-Driven Wound Closure

Mouse Pancreatic Islets Are Resistant to Indoleamine 2,3 Dioxygenase-Induced General Control Nonderepressible-2 Kinase Stress Pathway and Maintain Normal Viability and Function

Fibroblast mechanics in 3D collagen matrices☆

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