Epidermal growth factor therapy and wound healing — past, present and future perspectives

Hardwicke, Joseph; Schmaljohann, Dirk; Boyce, Dean E.; Thomas, David William

doi:10.1016/s1479-666x(08)80114-x

Cited by 208 publications

(180 citation statements)

References 28 publications

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“…EGF family members are primary growth factors involved in re-epithelialization during cutaneous wound healing (30,31). High levels of ␤1,6 GlcNAc branching in EGF-Rs of GnT-V Tg A, Western blot analysis of EGF-R after L 4 -PHA lectin immunoprecipitation of skin specimens from wild-type and GnT-V Tg mice (n ϭ 2/each group).…”

Section: Aberrant Glycosylation Of Egf-r Enhances Its Signaling In Gnmentioning

confidence: 99%

Enhanced Epithelial-Mesenchymal Transition-like Phenotype in N-Acetylglucosaminyltransferase V Transgenic Mouse Skin Promotes Wound Healing

Terao

Ishikawa

Nakahara

et al. 2011

Journal of Biological Chemistry

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N-Acetylglucosaminyltransferase V (GnT-V) catalyzes the ␤1,6 branching of N-acetylglucosamine on N-glycans. GnT-V expression is elevated during malignant transformation in various types of cancer. However, the mechanism by which GnT-V promotes cancer progression is unclear. To characterize the biological significance of GnT-V, we established GnT-V transgenic (Tg) mice, in which GnT-V is regulated by a ␤-actin promoter. No spontaneous cancer was detected in any organs of the GnT-V Tg mice. However, GnT-V expression was up-regulated in GnT-V Tg mouse skin, and cultured keratinocytes derived from these mice showed enhanced migration, which was associated with changes in E-cadherin localization and epithelial-mesenchymal transition (EMT). Further, EMT-associated factors snail, twist, and N-cadherin were up-regulated, and cutaneous wound healing was accelerated in vivo. We further investigated the detailed mechanisms of EMT by assessing EGF signaling and found up-regulated EGF receptor signaling in GnT-V Tg mouse keratinocytes. These findings indicate that GnT-V overexpression promotes EMT and keratinocyte migration in part through enhanced EGF receptor signaling.Oligosaccharide structure changes are detected following birth, differentiation, and carcinogenesis (1), and these changes are regulated by glycosyltransferases. In particular, N-acetylglucosaminyltransferase V (GnT-V) 3 plays an important role in carcinogenesis and tumor metastasis (2). To characterize the detailed molecular mechanisms underlying GnT-V-related tumor metastasis, we and other groups succeeded in purifying and cloning . In addition, we developed a sugar remodeling system of cancer cells and demonstrated the biological function of GnT-V in tumor metastasis through biochemical analysis of its target glycoproteins (6). Granovsky et al. (7) reported that mammary tumor growth and metastases induced by the polyomavirus middle T oncogene were considerably less in GnT-V-deficient mice than in littermate control mice. Cancer cells established from GnT-V-deficient mice showed lower cell growth and intracellular signaling than control mice because of aberrant glycosylation of growth factor receptors (8). Dennis et al. (9) also reported that sugar metabolism is critical to control the formation of ␤1,6 N-acetylglucosamine (GlcNAc), a product of GnT-V. In contrast, GnT-V is involved in negative regulation of T cell activation, leading to suppression of the autoimmune reaction (10). Recently, Mkhikian et al. (11) reported that genetic changes in glycosylation status for suppressing N-glycan branching are concerned with the incidence of multiple sclerosis. Our groups have studied biological functions of adhesion molecules such as cadherin and integrins in terms of N-glycan branching mediated by GnT-V and have found that GnT-V inhibits cell-cell/cell-matrix adhesion and promotes migration of cancer cells (12).Although GnT-V is known to be up-regulated in the early phase of carcinogenesis in many cancers (13), it is unclear whether GnT-V regulates the late ph...

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Section: Aberrant Glycosylation Of Egf-r Enhances Its Signaling In Gnmentioning

confidence: 99%

Enhanced Epithelial-Mesenchymal Transition-like Phenotype in N-Acetylglucosaminyltransferase V Transgenic Mouse Skin Promotes Wound Healing

Terao

Ishikawa

Nakahara

et al. 2011

Journal of Biological Chemistry

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“…However there is limited information to guide treatment of diabetic ulcers. 1 Growth factors play a very important part in the process of wound healing. Epidermal Growth Factor was discovered by an American Biochemist Stanley Cohen in 1986, for which he won Nobel Prize in physiology and medicine .…”

Section: Introductionmentioning

confidence: 99%

Epidermal Growth Factor Versus Conventional Wound Dressings In Treatment Of Diabetic Ulcers- A Comparative Study

Ramachandran¹,

Ramdas²

2017

IOSR JDMS

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“…It accelerates wound healing rates through enhancing synthesis of basement membrane and extracellular matrix components, cell motility, and proliferation. 14,15 Yet, the halflife of EGF in the body is too short to exert the biological activity effectively when applied via injection or in free form. In addition, accumulating evidences suggested that EGF is effective as an adjuvant but not as monotherapy for wound repair mainly due to its ineffective delivery and rapid proteolysis.…”

Section: Introductionmentioning

confidence: 99%

EGF and curcumin co-encapsulated nanoparticle/hydrogel system as potent skin regeneration agent

et al. 2016

IJN

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Wound healing is a complex multifactorial process that relies on coordinated signaling molecules to succeed. Epidermal growth factor (EGF) is a mitogenic polypeptide that stimulates wound repair; however, precise control over its application is necessary to reduce the side effects and achieve desired therapeutic benefits. Moreover, the extensive oxidative stress during the wound healing process generally inhibits repair of the injured tissues. Topical applications of antioxidants like curcumin (Cur) could protect tissues from oxidative damage and significantly improve tissue remodeling. To achieve much accelerated wound healing effects, we designed a novel dual drug co-loaded in situ gel-forming nanoparticle/hydrogel system (EGF-Cur-NP/H) which acted not only as a supportive matrix for the regenerative tissue, but also as a sustained drug depot for EGF and Cur. In the established excisional full-thickness wound model, EGF-Cur-NP/H treatment significantly enhanced wound closure through increasing granulation tissue formation, collagen deposition, and angiogenesis, relative to normal saline, nanoparticle/hydrogel (NP/H), Cur-NP/H, and EGF-NP/H treated groups. In conclusion, this study provides a biocompatible in situ gel-forming system for efficient topical application of EGF and Cur in the landscape of tissue repair.

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Epidermal growth factor therapy and wound healing — past, present and future perspectives

Cited by 208 publications

References 28 publications

Enhanced Epithelial-Mesenchymal Transition-like Phenotype in N-Acetylglucosaminyltransferase V Transgenic Mouse Skin Promotes Wound Healing

Enhanced Epithelial-Mesenchymal Transition-like Phenotype in N-Acetylglucosaminyltransferase V Transgenic Mouse Skin Promotes Wound Healing

Epidermal Growth Factor Versus Conventional Wound Dressings In Treatment Of Diabetic Ulcers- A Comparative Study

EGF and curcumin co-encapsulated nanoparticle/hydrogel system as potent skin regeneration agent

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