Enhancement of Wound Healing by Topical Treatment with Epidermal Growth Factor

Brown, Gregory L.; Nanney, Lillian B.; Griffen, Joseph; Cramer, Anne B.; Yancey, John M.; Curtsinger, Luke J.; Holtzin, Larry; Schultz, Gregory S.; Jurkiewicz, M. J.; Lynch, John B.

doi:10.1056/nejm198907133210203

Cited by 624 publications

(293 citation statements)

References 14 publications

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“…These growth cytokines are known to stimulate cell proliferation, migration, differentiation, cell survival, and protein synthesis, and have been shown to enhance healing of wounds 42, 43, 44, 45. Additionally, TIMP‐1, which was also upregulated, is an inhibitor of MMPs and is actively involved in tissue remodeling processes 46…”

Section: Discussionmentioning

confidence: 99%

Dehydrated human amnion/chorion membrane regulates stem cell activity in vitro

Massee

Chinn

Lei³

et al. 2015

J Biomed Mater Res

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Human‐derived placental tissues have been shown in randomized clinical trials to be effective for healing chronic wounds, and have also demonstrated the ability to recruit stem cells to the wound site in vitro and in vivo. In this study, PURION® Processed dehydrated human amnion/chorion membrane allografts (dHACM, EpiFix®, MiMedx Group, Marietta, GA) were evaluated for their ability to alter stem cell activity in vitro. Human bone marrow mesenchymal stem cells (BM‐MSCs), adipose derived stem cells (ADSCs), and hematopoietic stem cells (HSCs) were treated with soluble extracts of dHACM tissue, and were evaluated for cellular proliferation, migration, and cytokine secretion. Stem cells were analyzed for cell number by DNA assay after 24 h, closure of an acellular zone using microscopy over 3 days, and soluble cytokine production in the medium of treated stem cells was analyzed after 3 days using a multiplex ELISA array. Treatment with soluble extracts of dHACM tissue stimulated BM‐MSCs, ADSCs, and HSCs to proliferate with a significant increase in cell number after 24 h. dHACM treatment accelerated closure of an acellular zone by ADSCs and BM‐MSCs after 3 days, compared to basal medium. BM‐MSCs, ADSCs, and HSCs also modulated endogenous production of a number of various soluble signals, including regulators of inflammation, mitogenesis, and wound healing. dHACM treatment promoted increased proliferation and migration of ADSCs, BM‐MSCs, and HSCs, along with modulation of secreted proteins from those cells. Therefore, dHACM may impact wound healing by amplifying host stem cell populations and modulating their responses in treated wound tissues. © 2015 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 104B: 1495–1503, 2016.

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Section: Discussionmentioning

confidence: 99%

Dehydrated human amnion/chorion membrane regulates stem cell activity in vitro

Massee

Chinn

Lei³

et al. 2015

J Biomed Mater Res

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“…There are also common pathways, such as the extracellular regulated kinase (ERK) pathway of MAP kinases, which transduce signals upon activation of both EGF and FGF receptors (Karin et al, 1997). Furthermore, EGF and FGF-2 are able to promote regeneration processes, such as wound healing (Andree et al, 1994;Brown et al, 1989;Davidson and Broadley, 1991). It is remarkable that although sharing all these activities, the gene expression pattern the growth factors induce in one cell type is only partially overlapping.…”

Section: Introductionmentioning

confidence: 99%

The activation and composition of FiRE (an FGF-inducible response element) differ in a cell type- and growth factor-specific manner

1998

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The expression of the heparan sulfate proteoglycan, syndecan-1, is induced both in keratinocytes and in ®broblasts during development and tissue regeneration. Here we report that in keratinocytes the syndecan-1 gene was stimulated by EGF but not by FGF-2. In ®broblasts it was stimulated by FGF-2 but not by EGF. Likewise, the recently discovered FGF-inducible response element (FiRE) on the gene of syndecan-1 was stimulated by FGF-2 in ®broblasts and by EGF in keratinocytes, but not vice versa. The FiRE has two binding sites for an activator protein-1 (AP-1), one for an FGF-inducible nuclear factor (FIN-1) and one for an upstream stimulatory factor-1 (USF-1). The growth factorstimulated binding of these transcription factors, as well as their requirement for FiRE activation, varied between the two cell types. First, although AP-1s were required for activation of FiRE in both cell types, the binding of AP-1 to FiRE was increased by growth factor-stimulation only in ®broblasts and not in keratinocytes. Secondly, FiRE did not bind FIN-1 nor needed the FIN-1 binding site for EGF-stimulated activation in keratinocytes, in contrast to the FGF-stimulated activation of FiRE in ®broblasts. Thirdly, EGF, which did not activate FiRE in ®broblasts, failed to activate FIN-1 in these cells. Finally, an USF-1 binding site that was necessary for activation of FiRE in keratinocytes was not needed in ®broblasts. These data suggest mechanisms by which members of the EGF-and FGF-families can di erentially stimulate transcription through AP-1 regulated elements in a cell type-speci®c manner.

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“…EGF is known to be a key stimulator of epithelial cell growth and remodeling (7)(8)(9), and EGF also increases the mucosal barrier function and epithelial repair/ restitution processes in human and animals (6). For example, the addition of EGF enemas to mesalamine treatment in ulcerative colitis patients has been shown to increase the therapeutic response rate (6).…”

mentioning

confidence: 99%

The Insect Peptide CopA3 Increases Colonic Epithelial Cell Proliferation and Mucosal Barrier Function to Prevent Inflammatory Responses in the Gut

Kim

Hwang

Lee

et al. 2016

Journal of Biological Chemistry

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The epithelial cells of the gut form a physical barrier against the luminal contents. The collapse of this barrier causes inflammation, and its therapeutic restoration can protect the gut against inflammation. EGF enhances mucosal barrier function and increases colonocyte proliferation, thereby ameliorating inflammatory responses in the gut. Based on our previous finding that the insect peptide CopA3 promotes neuronal growth, we herein tested whether CopA3 could increase the cell proliferation of colonocytes, enhance mucosal barrier function, and ameliorate gut inflammation. Our results revealed that CopA3 significantly increased epithelial cell proliferation in mouse colonic crypts and also enhanced colonic epithelial barrier function. Moreover, CopA3 treatment ameliorated Clostridium difficile toxin As-induced inflammation responses in the mouse small intestine (acute enteritis) and completely blocked inflammatory responses and subsequent lethality in the dextran sulfate sodium-induced mouse model of chronic colitis. The marked CopA3-induced increase of colonocyte proliferation was found to require rapid protein degradation of p21 Cip1/Waf1 , and an in vitro ubiquitination assay revealed that CopA3 directly facilitated ubiquitin ligase activity against p21 Cip1/Waf1 . Taken together, our findings indicate that the insect peptide CopA3 prevents gut inflammation by increasing epithelial cell proliferation and mucosal barrier function.

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Enhancement of Wound Healing by Topical Treatment with Epidermal Growth Factor

Cited by 624 publications

References 14 publications

Dehydrated human amnion/chorion membrane regulates stem cell activity in vitro

Dehydrated human amnion/chorion membrane regulates stem cell activity in vitro

The activation and composition of FiRE (an FGF-inducible response element) differ in a cell type- and growth factor-specific manner

The Insect Peptide CopA3 Increases Colonic Epithelial Cell Proliferation and Mucosal Barrier Function to Prevent Inflammatory Responses in the Gut

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