• Imaging Science in Dentistry
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• v.30 no.1
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• pp.71-79
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• 2000

Purpose : This study was aimed to evaluate the cell cycle arrest and apoptosis induction after irradiation and epidermal growth factor (EGF) treatment in three human epithelial tumor cell lines (A431, Siha, KB). Materials and Methods: Single irradiation of 2, 5 and 10 Gy was done on three cell lines with 5.38 Gy/min dose rate using Cs-137 irradiator at room temperature. Also, EGF of 10 ng/ml was added immediately after 10 Gy irradiation. Cell growth was evaluated by counting the living cell number using a hemocytometer at 1 day, 2 days, 3 days, 4 days and 5 days after irradiation. Cell cycle arrest and apoptosis induction were assayed with the flow cytometry at 8 hours, 12 hours, 1 day, 2 days, 3 days, 4 days and 5 days after irradiation. Results : Growth of irradiated three cell lines were inhibited in proportion to radiation dose. EGF treatment after irradiation showed various results according to cell lines. On all cell lines, G2 arrest was detected after 8 hours and maximized after 12 hours or 1 day. Amount of G2 arrest was positively dose dependent. However, EGF showed no significant change on G2 arrest. G2 arrest was recovered with time at 2 Gy and 5 Gy irradiation. However, at 10 Gy irradiation, G2 arrest was continued. Apoptosis was detected at 10 Gy irradiation. On EGF treated group after irradiation, A431 and Siha cell lines showed slightly increased apoptosis but there was no statistically significant difference. KB cell line showed no marked change of apoptosis induction. Conclusion : Irradiation effects on cell cycle arrest and apoptosis induction in three human epithelial tumor cell lines, however epidermal growth factor doesn't effect on.

• Korean Journal of Animal Reproduction
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• v.21 no.2
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• pp.177-183
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• 1997

The present study examined the effects of epidermal growth factor(EGF) and transforming growth factor-$\alpha$(TGF-$\alpha$) on in vitro maturation of porcine follicular oocytes. Basic medium used TCM-HEPES, and oocytes cultured for 42 hours in vitro. The results obtained are as follows; 1. The nuclear maturation rates of EGF-treated groups(10ng/ml, 75.9% ; 30ng/ml, 69.2% ; 50ng/ml, 67.2% ; 100ng/ml, 71.0%) on the porcine oocytes cultured in medium without pFF in vitro were significantly(P<0.01) higher than those of non-treated group(57.1%). When the oocytes were cultured in media with 10%(v/v) pFF, the nuclear maturation rates of 30ng EGF/ml(77.1%) treated group were significantly(P<0.01) higher than those of non-(59.2%) and EGF-treated groups(10ng/ml, 65.4% ; 50ng/ml, 65.5% ; 100ng/ml, 70.4%). 2. The nuclear maturation rates of 30ng TGF-$\alpha$/ml treated group(71.9%) in media without pFF in vitro were significatnly(P<0.01) higher than those of non-(57.1%) and TGF-$\alpha$ treated groups(10ng/ml, 60.4% ; 50ng/ml, 65.4% ; 100ng/ml, 60.0%). When the oocytes were cultured in media with 10%(v/v) pFF, the nuclear maturation rates of 30 and 50ng TGF-$\alpha$/ml(77.4% and 79.6%) treated groups(10ng/ml, 64.2% ; 100ng/ml, 61.6%). 3. On the effect of EGF(30ng/ml) and/or TGF-$\alpha$(30ng/ml) treated groups in medium without pFF in vitro, the nuclear maturation rates indicated 57.3, 60.4, 75.9 and 79.7% in media with no EGF & TFG-$\alpha$, TGF-$\alpha$ only, EGF only nad EGF＋TGF-$\alpha$ treated groups, respectively. The nuclear maturation rates in medium with EGF only or EGF＋TGF-$\alpha$ were significantly(P<0.01) higher than those non- and TGF-$\alpha$ treated groups. When the oocytes were cultured in media with 10%(v/v) pFF, the nuclear maturation ratesof EGF＋TGF-$\alpha$ treated group(75.9%) were significantly(P<0.01) higher than those of non-(59.2%), TGF-$\alpha$ only (64.2%) and EGF only(69.4%) treated groups.

• Asian-Australasian Journal of Animal Sciences
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• v.29 no.1
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• pp.134-141
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• 2016

To investigate the role of polysaccharide from Acanthopanax senticosus (ASPS) in preventing lipopolysaccharide (LPS)-induced intestinal injury, 18 mice (at 5 wk of age) were assigned to three groups with 6 replicates of one mouse each. Mice were administrated by oral gavage with or without ASPS (300 mg/kg body weight) for 14 days and were injected with saline or LPS at 15 days. Intestinal samples were collected at 4 h post-challenge. The results showed that ASPS ameliorated LPS-induced deterioration of digestive ability of LPS-challenged mice, indicated by an increase in intestinal lactase activity (45%, p<0.05), and the intestinal morphology, as proved by improved villus height (20.84%, p<0.05) and villus height:crypt depth ratio (42%, p<0.05), and lower crypt depth in jejunum (15.55%, p<0.05), as well as enhanced intestinal tight junction proteins expression involving occludin-1 (71.43%, p<0.05). ASPS also prevented intestinal inflammation response, supported by decrease in intestinal inflammatory mediators including tumor necrosis factor ${\alpha}$ (22.28%, p<0.05) and heat shock protein (HSP70) (77.42%, p<0.05). In addition, intestinal mucus layers were also improved by ASPS, as indicated by the increase in number of goblet cells (24.89%, p<0.05) and intestinal trefoil peptide (17.75%, p<0.05). Finally, ASPS facilitated mRNA expression of epidermal growth factor (100%, p<0.05) and its receptor (200%, p<0.05) gene. These results indicate that ASPS can prevent intestinal mucosal barrier injury under inflammatory conditions, which may be associated with up-regulating gene mRNA expression of epidermal growth factor and its receptor.

• International Journal of Oral Biology
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• v.43 no.3
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• pp.161-169
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• 2018

We previously demonstrated that epidermal growth factor (EGF) enhances cell migration and invasion of breast cancer cells in a SMAD ubiquitination regulatory factor 1 (SMURF1)-dependent manner and that SMURF1 induces degradation of ${\beta}-catenin$ in C2C12 cells. However, the relationship between EGF-induced SMURF1 and ${\beta}-catenin$ expression in breast cancer cells remains unclear. So, we investigated if EGF and SMURF1 regulate ${\beta}-catenin$ expression in MDAMB231 human breast cancer cells. When MDAMB231 cells were incubated with EGF for 24, 48, and 72 hours, EGF significantly increased expression levels of SMURF1 mRNA and protein while suppressing expression levels of ${\beta}-catenin$ mRNA and protein. Overexpression of SMURF1 downregulated ${\beta}-catenin$ mRNA and protein, whereas knockdown of SMURF1 increased ${\beta}-catenin$ expression and blocked EGF-induced ${\beta}-catenin$ downregulation. Knockdown of ${\beta}-catenin$ enhanced cell migration and invasion of MDAMB231 cells, while ${\beta}-catenin$ overexpression suppressed EGF-induced cell migration and invasion. Furthermore, knockdown of ${\beta}-catenin$ enhanced vimentin expression and decreased cytokeratin expression, whereas ${\beta}-catenin$ overexpression decreased vimentin expression and increased cytokeratin expression. These results suggest that EGF downregulates ${\beta}-catenin$ in a SMURF1-dependent manner and that ${\beta}-catenin$ downregulation contributes to EGF-induced cell migration and invasion in MDAMB breast cancer cells.

• Tuberculosis and Respiratory Diseases
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• v.55 no.1
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• pp.21-30
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• 2003

Background : Mucin synthesis in airways has been reported to be regulated by the epidermal growth factor receptor (EGFR) system. Epidermal growth factor receptor transactivation was identified as a critical element in G-protein-coupled receptors (GPCRs)-induced mitogenic signaling. EGF receptor transactivation by G-protein-coupled receptors requires metalloproteinase cleavage of proHB-EGF. This study was hypothesized that lipopolysaccharide (LPS)-induced mucin production associates with epidermal growth factor receptor transactivation, and MUC5AC production associates with epidermal growth factor receptor transactivation by G-protein-coupled receptors that regulates by metalloproteinase. Method : MUC5AC mucin production was examined in NCI-H292 cells and MUC5AC protein synthesis was assessed using ELISA. For the evaluation of mechanism of LPS-induced MUC5AC production, $TNF{\alpha}$ was measured using ELISA with or without pretreatment of heterotrimeric G-protein inhibitor, mastoparan. MUC5AC protein was measure with pretreatment of polyclonal $TNF{\alpha}$ antibody or mastoparan on LPS-induced MUC5AC production. For the evaluation of relation of G-protein and MUC5AC production, G-protein stimulant, mastopara-7, or matrix metalloproteinase, ADAM10, was added to NCI-H292 cells. MUC5AC protein was measure with pretreatment of polyclonal EGF antibody on mastoparan-7-induced MUC5AC production. Results : LPS alone did not increase significantly MUC5AC production. LPS with $TNF{\alpha}$ induced dose-dependently MUC5AC production in NCI-H292 cells. LPS increased dose-dependently $TNF{\alpha}$ secretion, which was inhibited by mastoparan. LPS with $TNF{\alpha}$-induced MUC5AC production was inhibited by neutralizing polyclonal $TNF{\alpha}$ antibody, mastoparan or AG 1472. Mastoparan-7 or ADAM10 increased dose-dependently MUC5AC production, which was inhibited by polyclonal neutralizing EGF antibody. Conclusion : In LPS-induced MUC5AC synthesis, LPS causes $TNF{\alpha}$ secretion, which induces EGFR expression. EGFR tyrosine kinase phosphorylation result in MUC5AC production. EGF-R transactivation by G-protein-coupled receptors requires matrix metalloproteinase cleavage of proHB-EGF.

• YAKHAK HOEJI
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• v.40 no.4
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• pp.411-417
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• 1996

Epidermal growth factor(EGF), a potential healing agent for wounds and burns, has been formulated to topical gels with the hydrophilic polymers, Carbopol 934P. Physicochemical c haracteristics of the aqueous gels were evaluated by rheological properties and pH changes on storage. The gels were relatively stable at $4^{\circ}C$ and room temperature showing no changes in pH for two weeks, and revealed the rheogram of shear thinning plastic flow with the yield values in the range of 40 to 70dyne/$cm^2$. In vivo healing effects of different gel formulations have been compared with water-soluble and oleaginous ointments in full-thickness wound mouse model. The gel systems resulted in better wound healing effects than the other ointments. Furthermore, liposomal Carbopol gel has been developed by the addition of EGF-containing liposomal suspension into the Carbopol gel. The enhanced wound healing effects have been observed in the liposomal gel system, compared to the other gels and conventional ointments.

• Journal of Photoscience
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• v.9 no.2
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• pp.194-196
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• 2002

While ultraviolet radiation alters various cutaneous cell functions, little is known about photo-immunological and photobiological effects of infrared radiation (IR) on the skin except its local thermal effects. The fIrst part of this study demonstrated that single exposure of mouse skin to near IR (0.7 - 1.3 $\mu$m) reversibly suppressed the proliferating activity of the epidermis, the density of Langerhans cells, and the ability of skin to induce contact hypersensitivity reaction. The second part demonstrated that the rate of wound closure was significantly accelerated by repeated exposures in animal models. The production of transforming growth factor-$\beta$l and matrix metalloproteinase-2, which are responsible for the wound healing processes, was significantly upregulated by irradiation, as shown by enzyme immunoassay, zymography, and reverse transcription polymerase chain reaction. Thermal controls were negative. The results suggest that near-IR irradiation can modulate the epidermal proliferation and part of the skin immune system, and stimulate the wound healing processes, presumably by non-thermal effects.

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.415.3-416
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• 2002

To improve the stability of recombinant human epidermal growth factor (rhEGF) as therapeutic agent. the N-terminal PEGylated rhEGF (N-PEG-rhEGF) was prepared by site-specific bioconjugation and the stability was investigated in rat skin wound homogenates. Two different N-PEG-rhGEFs (N-PEG5K- and N-PEG20K-rhEGF) were successfully prepared with the yields of above 70%. The PEGylation site was directly confirmed by determining the molecular mass of Lys-C digested samples using MALDI- TOF MS. (omitted)

• Biotechnology and Bioprocess Engineering:BBE
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• v.2 no.2
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• pp.86-89
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• 1997

Epidermal growth factor(EGF) known as a urgastrone is a powerful mitogen with a wide variety of possibilities for medical usages. A mature EGF coding region was isolated from human prepro-EGF sequence by a conventional PCR and cloned into pQE vector in which the gene product was supposed to be expressed with 6$\times$His tag for the subsequent purification. The recombinant mature EGF was expressed in M15[Rep4], an Escherichia coli host strain, in amount of 30-40% of total proteins pressent in E. coli extract by the addition of isopropylthio-$\beta$-galactopyranoside (IPTG). The recombinant EGF purified using a Ni2+-NTA affinity colume chromatography was active in its ability to induce phosphorylation on tyrosine residues of several substrate proteins when murine NH3T3 and human MRC-5 fibroblast cells were stimulated with it. This work may provide the basic technology and information for the production of recombinant EGF.

• Journal of the Korea Society of Computer and Information
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• v.21 no.9
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• pp.101-106
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• 2016

The epidermal growth factor receptor(EGFR) protein kinase signaling is an important pathway in cancer development and recently reported that EGFR and its kinase domain molecules are mutated in various of cancers including head and neck cancer. Functional deregulation of EGFR due to mutations in coding exons and copy number amplification is the most common event in cancers, especially among receptor tyrosine kinases(TK). We have analyzed Korean oral squamous cell carcinomas (OSCC) cell lines for mutations in EGFRTK. Exons encoding the hot-spot regions in the TK domain of EGFR (exons 17 to 23) were amplified by using polymerase chain reaction(PCR) and sequenced directly. EGFR expression was also analyzed in 8 OSCC cell lines using western blotting. Data analysis of the EGFR exons 17 to 23 coding sequences did not show any mutations in the 8 OSCC cell lines that were analyzed. The absence of mutations indicate that protein overexpression might be responsible for activation rather than mutation.