EGF, a veteran of wound healing: highlights on its mode of action, clinical applications with focus on wound treatment, and recent drug delivery strategies

Shakhakarmi, Kanchan; Seo, Jeong-Sun; Lamichhane, Shrawani; Thapa, Chhitij; Lee, Sang-Kil

doi:10.1007/s12272-023-01444-3

Cited by 14 publications

(8 citation statements)

References 156 publications

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“…In the process of wound repair, the functions of growth factors include [9,10]: (1) Guide neutrophils and macrophages into the wound area to clear the necrotic tissue; (2) Promote proliferation of fibronuclear epidermal cells; (3) Promote the synthesis and release of the body's growth factors; (4) Elevate the formation of granulation tissue; (5) Promote the synthesis and accumulation of extracellular interstitial molecules; (6) Inhibit scar tissue hyperplasia. Among them, EGF has a strong ability to promote wound healing, promote cell division, promote the synthesis of extracellular matrix such as hyaluronic acid, fibulnexin, glycoprotein and hydroxyproline acid, and thus reduce scar hyperplasia [11].…”

Section: Introductionmentioning

confidence: 99%

Effect of collagen sponge combined with epidermal growth factor in repairing maxillofacial head and neck wounds in rats

Qian Wang,

Zhiyi Wei,

Tianlai Lin

et al. 2024

Cell Mol Biol (Noisy-le-grand)

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Section: Introductionmentioning

confidence: 99%

Effect of collagen sponge combined with epidermal growth factor in repairing maxillofacial head and neck wounds in rats

Qian Wang,

Zhiyi Wei,

Tianlai Lin

et al. 2024

Cell Mol Biol (Noisy-le-grand)

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“…Among these, EGF was employed in wound management and regenerative medicine since the late 1980s. Its widespread and enduring utilization is attributable to its exceptional tolerability and effectiveness [20].…”

Section: Introductionmentioning

confidence: 99%

The Effects of Ellagic Acid on Experimental Corrosive Esophageal Burn Injury

Keşim,

Aşır,

Ayaz

et al. 2024

CIMB

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This study aimed to investigate the antioxidant effect of Ellagic acid (EA) on wound healing in sodium hydroxide (NaOH)-induced corrosive esophageal burn injury. The interaction networks and functional annotations were conducted using Cytoscape software. A total of 24 Wistar albino rats were divided into control, corrosive esophageal burn (CEB) and CEB + EA groups. Burn injury was created by 20% NaOH and 30 mg/kg EA was per oral administered to rats. At the end of the 28-day experimental period, Malondialdehyde (MDA) content was measured. Esophageal tissue samples were processed for histological staining. The EA–target interaction network was revealed to be involved in regulating crucial cellular mechanisms for burn wound healing, with epidermal growth factor (EGF) identified as a central mediator. An increase in animal weight in the CEB + EA group was observed in the EA-treated group after CEB injury. Burn injury increased MDA content, but EA treatment decreased its level after CEB injury. Stenosis index, collagen degeneration, inflammation, fibrosis and necrosis levels were increased after CEB injury. EA treatment improved histopathology in the CEB + EA group compared to the CEB group. The expression of EGF was decreased in the CEB group but upregulated in the EA-treated group, suggesting a potential involvement of EA in cellular processes and tissue regeneration. EA, through its antioxidative and tissue regenerative properties, significantly contributes to alleviating the adverse effects of CEB injury, promoting wound healing.

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“…EGF stimulates keratinocyte proliferation and migration via a paracrine mechanism [ 1 , 3 , 6 ]. The proliferation and migration of keratinocytes, key events in skin wound healing, are induced through the activation of the phosphoinositide 3-kinases (PI3K)/protein kinase B (AKT) and mitogen-activated protein kinase kinases (MAPKs), which are EGF receptor signaling pathways [ 7 , 8 , 9 , 10 ]. EGF is found in many different sources, such as urine, tears, saliva, milk, and plasma [ 1 ]; however, it is difficult to isolate and purify from these sources, and EGF itself is not sufficiently stable for use in medical or cosmetic applications.…”

Section: Introductionmentioning

confidence: 99%

“…EGF is found in many different sources, such as urine, tears, saliva, milk, and plasma [ 1 ]; however, it is difficult to isolate and purify from these sources, and EGF itself is not sufficiently stable for use in medical or cosmetic applications. To overcome these drawbacks, many researchers have attempted to develop EGF delivery systems [ 9 , 11 , 12 , 13 ] and stable molecules that directly or indirectly activate EGF receptors [ 14 , 15 ]. G-protein-coupled receptor (GPCR) ligands, including lysophosphatidic acid (LPA), transactivate the EGF receptor by enhancing the tyrosine phosphorylation of the EGF receptor and stimulating the proliferation of keratinocytes [ 16 , 17 ].…”

Section: Introductionmentioning

confidence: 99%

Gintonin-Induced Wound-Healing-Related Responses Involve Epidermal-Growth-Factor-like Effects in Keratinocytes

Won,

Lee,

Choi

et al. 2023

IJMS

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Epidermal growth factor (EGF) receptor activation and related downstream signaling pathways are known to be one of the major mechanisms of the proliferation and migration of keratinocytes. The heparin-binding EGF-like growth factor (HB-EGF) binds to EGF receptors and stimulates keratinocyte proliferation and migration. Gintonin, a novel ginseng compound, is a lysophosphatidic acid (LPA) receptor ligand. Gintonin has skin-wound-healing effects. However, the underlying mechanisms for these gintonin actions remain unclear. In this study, we aimed to elucidate the involvement of EGFRs in gintonin-induced wound repair in HaCaT keratinocytes. In this study, a water-soluble tetrazolium salt-based assay, a modified Boyden chamber migration assay, and immunoblotting were performed. Gintonin increased EGF receptor activation in HaCaT cells. However, the gintonin-induced phosphorylation of the EGF receptor was markedly reduced via treatment with the LPA inhibitor Ki16425 or the EGF receptor inhibitor erlotinib. Gintonin-enhanced proliferation and migration were blocked by the EGF receptor inhibitors (erlotinib and AG1478). Additionally, gintonin stimulated the expression and release of HB-EGF in HaCaT cells. EGF receptor inhibitors blocked gintonin-enhanced HB-EGF expression. These results indicate that the wound-healing effects of gintonin are closely related to the collaboration between EGF receptor activation and HB-EGF release-mediated downstream signaling pathways.

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EGF, a veteran of wound healing: highlights on its mode of action, clinical applications with focus on wound treatment, and recent drug delivery strategies

Cited by 14 publications

References 156 publications

Effect of collagen sponge combined with epidermal growth factor in repairing maxillofacial head and neck wounds in rats

Effect of collagen sponge combined with epidermal growth factor in repairing maxillofacial head and neck wounds in rats

The Effects of Ellagic Acid on Experimental Corrosive Esophageal Burn Injury

Gintonin-Induced Wound-Healing-Related Responses Involve Epidermal-Growth-Factor-like Effects in Keratinocytes

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