The fibronectin synergy site modulates TGF-β-dependent fibroblast contraction

Meckmongkol, Teerin T.; Harmon, Robert M.; McKeown‐Longo, Paula J.; Water, Livingston Van De

doi:10.1016/j.bbrc.2007.06.121

Cited by 33 publications

(23 citation statements)

References 22 publications

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“…It is also involved in up‐regulating the angiogenic growth factor VEGF 107 . In addition, in vitro studies show TGF‐β1 playing a role in wound contraction by facilitating fibroblast contraction of the collagen matrix 108 …”

Section: Transforming Growth Factor‐β (Tgf‐β) Familymentioning

confidence: 99%

“…107 In addition, in vitro studies show TGF-b1 playing a role in wound contraction by facilitating fibroblast contraction of the collagen matrix. 108 During reepithelialization, TGF-b1 shifts keratinocyte integrin expression toward a more migratory phenotype. 62 There are conflicting data as to the role of TGF-b1 in keratinocyte proliferation.…”

Section: Transforming Growth Factor-b (Tgf-b) Familymentioning

confidence: 99%

See 1 more Smart Citation

PERSPECTIVE ARTICLE: Growth factors and cytokines in wound healing

Barrientos

Stojadinović

Golinko

et al. 2008

Wound Repair Regeneration

3,057

2,478

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Wound healing is an evolutionarily conserved, complex, multicellular process that, in skin, aims at barrier restoration. This process involves the coordinated efforts of several cell types including keratinocytes, fibroblasts, endothelial cells, macrophages, and platelets. The migration, infiltration, proliferation, and differentiation of these cells will culminate in an inflammatory response, the formation of new tissue and ultimately wound closure. This complex process is executed and regulated by an equally complex signaling network involving numerous growth factors, cytokines and chemokines. Of particular importance is the epidermal growth factor (EGF) family, transforming growth factor beta (TGF‐β) family, fibroblast growth factor (FGF) family, vascular endothelial growth factor (VEGF), granulocyte macrophage colony stimulating factor (GM‐CSF), platelet‐derived growth factor (PDGF), connective tissue growth factor (CTGF), interleukin (IL) family, and tumor nerosis factor‐α family. Currently, patients are treated by three growth factors: PDGF‐BB, bFGF, and GM‐CSF. Only PDGF‐BB has successfully completed randomized clinical trials in the Unites States. With gene therapy now in clinical trial and the discovery of biodegradable polymers, fibrin mesh, and human collagen serving as potential delivery systems other growth factors may soon be available to patients. This review will focus on the specific roles of these growth factors and cytokines during the wound healing process.

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Section: Transforming Growth Factor‐β (Tgf‐β) Familymentioning

confidence: 99%

Section: Transforming Growth Factor-b (Tgf-b) Familymentioning

confidence: 99%

PERSPECTIVE ARTICLE: Growth factors and cytokines in wound healing

Barrientos

Stojadinović

Golinko

et al. 2008

Wound Repair Regeneration

3,057

2,478

View full text Add to dashboard Cite

show abstract

“…In such cells, FN also mediates Rho-stimulated cellular contraction. In a wound-healing model in which fibroblasts are seeded on FNcoated polyacrylamide gels, Meckmongkol et al identified both the FN synergy site and TGF␤1-mediated Rho activation as crucial contributors in FN-mediated cell contraction (Meckmongkol et al, 2007). Bernstein et al recently identified another player in the myofibroblast transition; they implicated uPAR cleavage as a crucial step in the TGF␤1-mediated transition of fibroblasts into myofibroblasts (Bernstein et al, 2007).…”

Section: Ecm Remodeling and Tensionmentioning

confidence: 99%

Extracellular matrix dynamics in development and regenerative medicine

Daley

Peters

Larsen

2008

Journal of Cell Science

868

716

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The extracellular matrix (ECM) regulates cell behavior by influencing cell proliferation, survival, shape, migration and differentiation. Far from being a static structure, the ECM is constantly undergoing remodeling – i.e. assembly and degradation – particularly during the normal processes of development, differentiation and wound repair. When misregulated, this can contribute to disease. ECM assembly is regulated by the 3D environment and the cellular tension that is transmitted through integrins. Degradation is controlled by complex proteolytic cascades, and misregulation of these results in ECM damage that is a common component of many diseases. Tissue engineering strives to replace damaged tissues with stem cells seeded on synthetic structures designed to mimic the ECM and thus restore the normal control of cell function. Stem cell self-renewal and differentiation is influenced by the 3D environment within the stem cell niche. For tissue-engineering strategies to be successful, the intimate dynamic relationship between cells and the ECM must be understood to ensure appropriate cell behavior.

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“…Thus the hyperproliferation of keratinocytes seen in N-WASP FKO is probably not the sole reason for faster wound healing in N-WASP FKO . Upon injury the fibroblasts promotes wound healing by several mechanisms3141, the fibroblasts proliferate, synthesis collagen and differentiate to myofibroblasts which helps in wound healing by contracting the wound3142. Thus we analyzed the collagen gel contraction properties of WT and N-WASP deficient fibroblasts by TGFβ treatment of cells embedded in collagen matrix.…”

Section: Discussionmentioning

confidence: 99%

Conditional knockout of N-WASP in mouse fibroblast caused keratinocyte hyper proliferation and enhanced wound closure

Jain

Kalailingam

Tsuiki

et al. 2016

Sci Rep

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Neural-Wiskott Aldrich Syndrome Protein (N-WASP) is expressed ubiquitously, regulates actin polymerization and is essential during mouse development. We have previously shown that N-WASP is critical for cell-ECM adhesion in fibroblasts. To characterize the role of N-WASP in fibroblast for skin development, we generated a conditional knockout mouse model in which fibroblast N-WASP was ablated using the Cre recombinase driven by Fibroblast Specific Protein promoter (Fsp-Cre). N-WASPFKO (N-WASPfl/fl; Fsp-cre) were born following Mendelian genetics, survived without any visible abnormalities for more than 1 year and were sexually reproductive, suggesting that expression of N-WASP in fibroblast is not critical for survival under laboratory conditions. Histological sections of N-WASPFKO mice skin (13 weeks old) showed thicker epidermis with higher percentage of cells staining for proliferation marker (PCNA), suggesting that N-WASP deficient fibroblasts promote keratinocyte proliferation. N-WASPFKO mice skin had elevated collagen content, elevated expression of FGF7 (keratinocyte growth factor) and TGFβ signaling proteins. Wound healing was faster in N-WASPFKO mice compared to control mice and N-WASP deficient fibroblasts were found to have enhanced collagen gel contraction properties. These results suggest that N-WASP deficiency in fibroblasts improves wound healing by growth factor-mediated enhancement of keratinocyte proliferation and increased wound contraction in mice.

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The fibronectin synergy site modulates TGF-β-dependent fibroblast contraction

Cited by 33 publications

References 22 publications

PERSPECTIVE ARTICLE: Growth factors and cytokines in wound healing

PERSPECTIVE ARTICLE: Growth factors and cytokines in wound healing

Extracellular matrix dynamics in development and regenerative medicine

Conditional knockout of N-WASP in mouse fibroblast caused keratinocyte hyper proliferation and enhanced wound closure

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