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Biomedical subjects

C Y Wu-Wang

Publications and source records attributed to C Y Wu-Wang.

At least 19 recordsLinked to original sources
PubMed1997

Time-dependent alteration of epidermal growth factor receptor in rat stomach by ethanol feeding.

This study investigated the time-dependent effects of ethanol (EtOH) feeding on epidermal growth factor binding and epidermal growth factor-mediated functions in the stomach. Adult male rats were fed either an isocaloric control or EtOH-containing liquid diet (36% total calories as EtOH) for 2, 4 and 6 weeks. At the end of each feeding period, animals were sacrificed and the stomach was dissected for the sample preparation. EtOH caused a time-dependent alteration (r = 0.89) of the 125I-epidermal growth factor binding to the gastric mucosal membrane (% control: week 2, 114%; week 4, 64%* and week 6, 45%*, n = 5, *P < 0.05). Protein kinase analysis also showed that EtOH caused a time-dependent decrease of epidermal growth factor-stimulated autophosphorylation of epidermal growth factor receptor protein (180 kDa) during three feeding periods. Western blot analysis, using anti-tyrosine phosphorylated epidermal growth factor receptor (active form) antibody, revealed a major immunoreactive protein band (180 kDa) in all samples pre-incubated with 1 microM epidermal growth factor. Consistent with data from kinase analysis, treatment of EtOH decreased the immunoreactivity of the active form of epidermal growth factor receptor (180 kDa) in the stomach. In conclusion, EtOH feeding caused a time-dependent alteration of epidermal growth factor receptor in the stomach, which may be one of the mechanisms underlying the gastric pathology associated with alcohol abuse.

Animals↗
PubMed1996

Effects of in vivo treatments of nicotine and benzo[a]pyrene on the epidermal growth factor receptor in hamster buccal pouch.

This study was conducted to investigate the effects of two major ingredients in cigarette smoke, benzo-alpha-pyrene (BP) and nicotine (Nic), on epidermal growth factor (EGF) receptor in hamster buccal pouch. Adult male Syrian hamsters were treated by apically swabbing the buccal pouch with mineral oil (Control), 0.5 microgram/ml of BP, Nic or BP+Nic in mineral oil, twice a day, 5 days a week for 4 weeks. The BP+Nic treatment resulted in a significant reduction of submandibular gland (SG) EGF (Control vs. BP+Nic, 6.93 +/- 1.31 vs. 4.77 +/- 0.26* ng/g wet tissue, mean +/- S.D., n=5,*P < 0.05). Treatment with BP or Nic also caused a reduction, although not statistically significant, of EGF in SG extract. For the receptor study, all treatments significantly increased [125I]EGF binding to membrane preparations of buccal pouch as compared to Control (Control, BP, Nic, BP+Nic; 12.2 +/- 0.9, 20.5 +/- 2.2*, 17.0 +/- 1.3*, 21.2 +/= 1.6* fmol/mg prot. (mean +/- S.E.M.), n=5, P < 0.05). Scatchard analysis revealed that the higher EGF binding to the BP+Nic-treated sample was due to the higher number of receptors, but not higher affinity. Data from protein kinase study indicate that EGF stimulated phosphorylation of 170- and 150-kDa proteins in buccal membrane preparations. Treatment of BP+Nic resulted in reductions in EGF-stimulated phosphorylation of 170- and 150-kDa proteins by 19 and 72%, respectively. The present study has established an animal model which will benefit investigation of the mechanism by which tobacco alters the EGF receptor in oral buccal mucosa.

Animals↗
PubMed1996

Benzo[a]pyrene and nicotine alter prostaglandin E2 receptor and its functions in hamster buccal mucosa.

This study investigated the in vivo effect of benzo[a]pyrene (BP) and nicotine (NC) on prostaglandin E2 (PGE2) receptor and its cellular responses in hamster buccal mucosa. Adult male Syrian hamsters were treated by apical swabbing the pouch with mineral oil (control), or 1 mM BP + NC, twice/day, 3 times/week, for 8 weeks. The BP + NC treatment significantly decreased the specific binding of PGE2 to buccal mucosal membranes (12.8 +/- 0.14 vs 8.7 +/- 1.13 fmol/mg protein; control vs. BP + NC; mean +/- S.D., n=6, P < 0.05). Scatchard analysis revealed that the reduction of receptor binding might be due to an alteration of the receptor binding properties, such as increase of the dissociation constant (Kd, 1.08 vs. 4.20 nM; control vs. BP + NC) and elimination of the low-affinity binding site. The addition of 16,16-dimethyl PGE2 (DMPGE2) into the control buccal tissue caused a 36% decrease of the overall protein synthesis. In contrast, DMPGE2 enhanced the [35S]methionine incorporation into several major proteins (i.e., 150, 120, 90, 75, 55, 38 and 26 kDa) in the BP + NC group. DMPGE2 showed no effect on DNA synthesis in both groups. Our data demonstrated that BP + NC in vivo altered PGE2 receptor properties and cellular functions in hamster buccal pouch.

16,16-Dimethylprostaglandin E2↗
PubMed1996

Epidermal growth factor in gingival crevicular fluid and its binding capacity in inflamed and non-inflamed human gingiva.

Epidermal growth factor (EGF) is a pro-inflammatory small peptide (6000 Da) with a variety of biological activities including stimulation of cell differentiation and mediation of proteolysis by binding to its specific receptor on the cell surface. The purpose of this study was to determine the levels of EGF in gingival crevicular fluid (GCF) and the EGF-binding capacity to its receptor in gingival tissue. The GCF samples were collected from six patients by inserting paper strips into shallow (< 5 mm) and deep pockets (> or = 5 mm) for 30 s. The strips were soaked in 0.2 M acetate for extraction and the EGF in the supernatants was analysed by radioimmunoassay. To determine the binding capacity of EGF to its receptor, inflamed gingival tissues (pocket depth > or = 5 mm, Gingival Index = 1, 2 or 3) were collected during periodontal flap surgery and non-inflamed gingival tissues (pocket depth < 5 mm, Gingival Index = 0) were collected during surgical "crown lengthening' for aesthetic purposes. The tissues were pooled by group, homogenized for membrane preparation and the supernatants obtained after centrifugation were used in a 125IEGF binding assay. To determine the effect of inflammation on gingival EGF receptor, inflamed and non-inflamed gingival tissues were collected from six patients and prepared similarly to the binding assay. Gingival preparations were then electrophoresed for Western blot analysis with EGF receptor antiserum. The EGF level in GCF was significantly lower (P < 0.05) in the samples collected from pockets > or = 5 mm (0.9 +/- 0.6 ng/ml) than in those from pockets < 5 mm (2.4 +/- 2.1 ng/ml). The average Gingival Index was higher (2.6 +/- 0.6) in pockets > or = 5 mm than in pockets < 5 mm (1.4 +/- 1.0). Specific binding of 125I-EGF to its receptor in inflamed gingiva was 2.7-fold higher than in non-inflamed gingiva (14.4 +/- 4.9 vs 5.4 +/- 1.8 fmol/g wet tissue). Western blot analysis showed two major immunoreactive bands (180 and 120 kDa), which represent EGF receptor and its degradation products, in inflamed gingiva. The findings show that inflammation activates EGF binding capacity in gingiva and that the up-regulation of EGF receptor in inflamed gingiva might be associated with a lowered concentration of EGF in GCF produced adjacent to inflamed gingiva. This up-regulation of EGF receptor during inflammation might be an important mechanism in the pathogenesis of periodontal disease.

Blotting, Western↗
PubMed1995

Decreased levels of salivary prostaglandin E2 and epidermal growth factor in recurrent aphthous stomatitis.

Prostaglandin E2 and epidermal growth factor are two important cytoprotective compounds in saliva. This study investigated their salivary levels in controls and individuals with minor recurrent aphthous stomatitis. The development of recurrent aphthous stomatitis was divided into three stages: (1) early active stage (mucosal redness); (2) active stage (mucosal ulceration); (3) convalescent stage. Unstimulated mixed saliva was collected from each volunteer. Salivary prostaglandin E2 and epidermal growth factor concentrations were determined by radioimmunoassay. Their levels (mean +/- SEM) were significantly lower during the active stage of ulceration as compared to the control: (a) for prostaglandin E2, 200 +/- 55 versus 73 +/- 11 pg/mg salivary protein (p < 0.01), 447 +/- 123 versus 112 +/- 19 pg/ml saliva (p < 0.01), 215 +/- 30 versus 63 +/- 12 pg/min salivary flow (p < 0.01), control (n = 12) versus active stage (n = 15); (b) for epidermal growth factor, 1.09 +/- 0.17 versus 0.67 +/- 0.17 ng/mg salivary protein (p < 0.05); 2.51 +/- 0.53 versus 0.84 +/- 0.19 pg/ml saliva (p < 0.05), 1.24 +/- 0.26 versus 0.41 +/- 0.09 pg/min salivary flow (p < 0.05), control (n = 12) versus active stage (n = 12). Salivary prostaglandin E2 and epidermal growth factor showed stage-dependent alterations during the development of the stomatitis. The prostaglandin E2 concentration decreased significantly during the active stage of ulceration, and then increased significantly during the convalescent stage. However, the recovery of salivary epidermal growth factor after the ulceration was slower than that of the prostaglandin E2. It is suggested that the diminution of prostaglandin E2 and epidermal growth factor in the saliva may be associated with the ulcer development.

Adult↗
PubMed1994

Biochemical characterization of epidermal growth-factor receptor in Syrian hamster buccal pouch.

Binding of [125I]-epidermal growth factor (EGF) to the membrane of the adult hamster buccal pouch was specific and protein concentration dependent, and was significantly higher than that of rat buccal tissue (hamster versus rat; 12.1 +/- 0.9 versus 9.77 +/- 0.22 fmol/mg protein, mean +/- SD, n = 5, p < 0.01). The higher binding was due to a higher receptor number (Bmax). Western blot analysis using anti-EGF receptor antibody revealed four immunoreactive protein bands of 170, 150, 116 and 55 kDa in hamster buccal membrane preparations. In a separate experiment, the EGF concentration in the phosphate-buffered saline extract of the hamster submandibular gland was determined by radioimmunoassay; the level was significantly much lower (p < 0.01) than that of rat or mouse (hamster, rat, mouse; 24.2 +/- 2.6, 123 +/- 17, 5950 +/- 171 ng/g wet tissue; mean +/- SD, n = 3). The findings suggest that hamster buccal pouch is particularly well suited to the study of the biological functions of oral EGF receptor.

Animals↗
PubMed1993

Effects of benzo(a)pyrene and nicotine on prostaglandin synthesis in buccal pouch and submandibular glands of the Syrian hamster.

Adult male Syrian hamsters were treated by swabbing the apex of the buccal pouch with corn oil (control, C), 1 mM benzo(a)pyrene (BP), nicotine (NC), or BP+NC in corn oil, twice daily, 5 days a week. After a 4-week treatment, the pouches and submandibular glands were dissected and used for the determination of endogenous prostaglandin (PG) production and studies on in vitro PG synthesis. Of the three PGs analysed (PGE2, PGF2 alpha and 6-keto-PGF1 alpha), PGE2 was predominant in the pouch and the glands. BP or NC alone had only a weak effect on PG synthesis in both tissues. However, the combination of BP and NC had a synergistic effect, causing diminished PG synthesis in both tissues. In buccal pouch, BP+NC significantly decreased the concentrations of endogenous PGE2 and PGF2 alpha (PGE2: 0.669 +/- 0.254 versus 1.698 +/- 0.460, PGF2 alpha: 0.273 +/- 0.090 versus 0.625 +/- 0.272 ng/g tissue; BP+NC versus C; mean +/- SD, n = 5, p < 0.05). Similarly significant results were also found for in vitro PG synthesis (PGE2: 0.541 +/- 0.249 versus 1.399 +/- 0.340, PGF2 alpha: 1.045 +/- 0.428 versus 2.133 +/- 0.510 ng/g tissue; BP+NC versus C; mean +/- SD, n = 5, p < 0.05). In submandibular glands, BP+NC significantly diminished the concentration of endogenous PGE2 (1.183 +/- 0.175 versus 2.379 +/- 0.488 ng/g tissue; BP+NC versus C; mean +/- SD, n = 5, p < 0.05). The synthesis of 6-keto-PGF1 alpha in both tissues, and the synthesis of PGF2 alpha in submandibular gland, were slightly decreased with all treatments.

6-Ketoprostaglandin F1 alpha↗
PubMed1993

Expression of prostaglandin E2 receptor in hamster buccal pouch: effect of benzo (a) pyrene and nicotine.

Prostaglandin E2 (PGE2) plays an important role in the maintenance of oral mucosal integrity. In this study, we characterized PGE2 receptor binding in the buccal mucosa of Syrian hamster and assessed the effect of nicotine (NC) and benzo (a) pyrene (BP), the two major ingredients in cigarette smoke, on this receptor. Adult male animals were treated for 4 weeks by apical swabbing of the buccal pouch with corn oil (control, C), 1 mM NC, BP, or NC + BP in corn oil, twice a day, 5 days a week. The results obtained with the untreated group revealed the presence of a specific PGE2 receptor consisting of two binding sites (high affinity with Kd = 1.52 nM and Bmax = 37 fmol/mg protein and low affinity with Kd = 813 nM and Bmax = 1.29 pmol/mg protein). The treatment with NC, BP, and NC + BP caused a significant decrease in PGE2 receptor binding (specific binding: 10.20 +/- 0.42, 6.84 +/- 1.32**, 6.58 +/- 0.67** and 5.88 +/- 1.03** fmol/mg protein; C, NC, BP, and NC+BP, respectively; Mean +/- SD, n = 5, **p < 0.01). The data suggest that decreased receptor binding for PGE2 in the buccal mucosa may be the cause for the adverse effect of cigarette smoke on the health of oral mucosa.

6-Ketoprostaglandin F1 alpha↗
PubMed1992

Effect of cigarette smoking on salivary epidermal growth factor (EGF) and EGF receptor in human buccal mucosa.

The mouth acts as a primary target for cigarette smoke which is associated with several oral diseases and cancer. The present study investigated the effect of cigarette smoking on salivary EGF and the buccal EGF receptor. Samples of whole saliva and buccal biopsy were obtained from 15 healthy volunteers (10 smokers and 5 non-smokers). The smokers smoked 20 or more cigarettes/day for more than 5 years. Salivary cotinine (a major metabolite of nicotine) was determined by radioimmunoassay (RIA). The salivary cotinine level was consistent with the self-reported smoking status (smokers, 106-530 ng/ml saliva; non-smokers, < 2 ng/ml saliva). As compared to the non-smokers, the salivary EGF concentration (determined by RIA) was 32% lower in those smokers whose salivary cotinine level was 250 ng/ml or higher (non-smokers, 2.21 +/- 0.16; smokers, 1.57 +/- 0.09 ng/ml saliva; mean +/- S.E.M., P < 0.01). There was no significant difference in 125I-labeled EGF binding to the buccal receptor between the two groups. However, EGF stimulated the autophosphorylation of a 170-kDa protein band in the sample of non-smokers, but not in the smokers. The immunoblot analysis using anti-EGF receptor antibody indicated that the smoking-related deficiency in EGF receptor autophosphorylation was due to the functional alteration of the receptor proteins. In conclusion, cigarette smoking reduces the salivary EGF level and impairs the function of buccal EGF receptor, which may be associated with the pathology of smoking-related oral disease.

Blotting, Western↗
PubMed1992

Effect of ethanol on prostaglandin E2 receptor in rat submandibular salivary glands.

The dose-dependent effects of acute ethanol treatment on the prostaglandin E2 (PGE2) receptor in submandibular salivary glands was investigated. Rat submandibular-gland segments were preincubated with Dulbecco's modified Eagle's medium in the absence and the presence of various concentrations of ethanol (0.1-5%). After incubation, membranes were prepared and assayed for PGE2 receptor binding using [3H]-PGE2. Ethanol had no effect on receptor binding at concentrations below 1%, but binding was stimulated by higher concentrations. A 30% increase in binding occurred with 2.5% ethanol and 50% with 5% ethanol. This increase was due to an alteration of the binding characteristics. Scatchard analysis of the data from the control and 5% ethanol groups revealed that the ethanol-induced increase in PGE2 receptor binding was mainly due to a 26 and 58% decrease in the dissociation constant (Kd) for the high- and low-affinity binding sites, respectively. A 31% decrease of binding capacity (Bmax) was also observed in the low-affinity binding sites. The results demonstrate that PGE2 receptor binding in submandibular glands is not altered by acute treatment with ethanol at physiological doses. The receptor binding is also relatively stable on pretreatment with 1% ethanol. It is suggested that the increase of receptor binding induced by high concentrations of ethanol may be a spontaneous response to the decrease of PGE2 synthesis in the tissues.

Animals↗
PubMed1992

Ethanol-induced structural and functional alterations of epidermal growth factor receptor in buccal mucosa.

1. Ethanol treatment caused a 47% decrease in [125I]EGF binding to the membrane preparations of buccal mucosa resulting from the decrease of binding sites rather than the affinity of high affinity receptor. 2. The immunoblot revealed a protein band of 170 kDa in the control sample, while a barely detectable 200 kDa protein was observed in the ethanol-treated sample. 3. Protein kinase assays using [32P]ATP as probe showed an EGF-stimulated phosphorylation band of 170 kDa in the control but not in ethanol-treated sample. 4. Ethanol did not change the basal incorporation of [3H]thymidine and [35S]methionine, but caused a 38% and 57% decrease of EGF-stimulated thymidine and methionine incorporation, respectively. 5. The data suggest that EtOH decreases EGF receptor binding through modification of the receptor molecule, thereby impairing receptor kinase activity and its physiological function.

Animals↗
PubMed1992

Benzo[a]pyrene and nicotine impair epidermal growth factor mediated cellular functions of buccal mucosa.

This study investigated the effect of two major ingredients in cigarette smoke, benzo[a]pyrene (BP) and nicotine, on epidermal growth factor (EGF) receptor binding and EGF-mediated cellular functions in rat buccal mucosa. Rat buccal tissue was incubated in DMEM in the absence (control) and presence of 10 microM BP or nicotine for 2.5 h at 25 degrees C. There were no significant differences in [125I]EGF binding to the buccal mucosal membranes between the control and treatment groups. Protein tyrosine kinase assay showed that EGF stimulated phosphorylation of a 170-kDa protein band in the controls, but not in the BP- and nicotine-treated samples. The basal [3H]thymidine incorporations were not significantly different between the groups. Nevertheless, addition of 5 nM EGF increased [3H]thymidine incorporation by 22% in the control, but not in the BP- or nicotine-treated group. The results demonstrate that BP and nicotine change the buccal mucosal functions associated with alteration of EGF receptor.

Animals↗
PubMed1992

Cigarette smoking reduces human salivary eicosanoids.

The effect of cigarette smoking on salivary eicosanoid levels was investigated in 10 smoker and 10 non-smoker volunteers. The smokers consumed an average of 20 cigarettes/day for the past 5 years or longer. The smoking status was validated by salivary cotinine level. Eicosanoids were extracted from saliva with ethanol, and the radioimmunoassay was performed to determine the concentrations of four major eicosanoids, i.e. prostaglandin E2 (PGE2), PGF2 alpha, 6-sulphidopeptide-containing leukotrienes (LTs) and 12-hydroxyeicosatetraenoic acid (12-HETE). The levels of PGE2, PGF2 alpha, and LTs were significantly lower in the saliva of smokers as compared to that of the non-smokers (1.74 +/- 0.32 vs 2.41 +/- 0.64, p = 0.006; 0.36 +/- 0.12 vs 0.54 +/- 0.18, p = 0.04; 2.24 +/- 0.96 vs 4.92 +/- 1.29, p = 0.006; mean +/- SD, ng/ml saliva). No significant differences were found in the levels of 12-HETE between the two groups. The results suggest that cigarette smoking reduces the concentrations of both the cyclooxygenase and 5-lipoxygenase products in saliva.

Cotinine↗
PubMed1991

Prostaglandin E2 receptor of rat submandibular salivary glands.

The binding characteristics of the PGE2 receptor were investigated in membrane preparations from these glands. Specific [3H]PGE2 binding was linear as a function of the membrane protein concentration and reached steady state by 40 min of incubation at 37 degrees C under neutral pH. Scatchard analysis of the binding data produced a curvilinear plot with a Kd of 0.18 nM and Bmax of 1.02 fmol/mg protein for the high-affinity binding sites, and a Kd of 181 nM and Bmax of 5.72 pmol/mg protein for the low-affinity binding sites. A competitive displacement study indicated that the receptor was specific for prostaglandins of the E series. The study is the first to demonstrate the presence of the PGE2 receptor in rat submandibular gland and to provide its biochemical features.

Animals↗
PubMed1991

Impairment by ethanol of prostaglandin production in rat salivary glands.

Sublingual salivary acini and submandibular tissue were incubated in DMEM medium in the presence of various concentrations (0-5%) of ethanol and the content of the three major prostaglandins, PGE2, PGF2 alpha and 6-keto-PGF1 alpha, were determined by radioimmunoassay. In In the sublingual gland, ethanol caused a decrease in PGE2 and PGF2 alpha levels, but had no effect on 6-keto-PGF1 alpha, while all three prostaglandins were affected in the submandibular gland. At 2.5% ethanol, the production of PGF2 alpha and PGE2 in sublingual gland decreased by 10% and reached maximum inhibition at 5% ethanol, at which concentration there was a 20 and 30% decrease in their levels. In submandibular gland, 2.5% ethanol caused a 20% decrease in PGE2, 30% in PGF2 alpha and 50% in 6-keto-PGF1 alpha; 40% inhibition in PGE2, 57% in 6-keto-PGF1 alpha and 65% in PGF2 alpha occurred in the presence of 5% ethanol. These findings suggest that alcohol impairs the function of salivary glands by inhibiting prostaglandin production.

6-Ketoprostaglandin F1 alpha↗
PubMed1991

Effect of cholesterol deprivation on piglet small intestine and serum lipids.

Using the neonatal piglet, the effects of dietary cholesterol deprivation on growth, intestinal enzyme activity, intestinal and hepatic 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMG-CoA reductase), and serum lipid were studied. Six litters of piglets were randomly assigned to one of two feeding regimens: restricted (800 ml of formula/24 h) versus unrestricted (1,200 ml of formula/24 h). Within litters, piglets were separated by sex, then randomly assigned to a formula containing low cholesterol (less than 2 mg/dl) or high cholesterol (145 mg/dl). Piglets were fed for 2 weeks. Male piglets in the restricted low cholesterol group gained significantly less weight per milliliter of formula than the restricted high cholesterol males. No effect was observed in the females. Microvillus membrane lactase activity was greater in males fed a high versus low cholesterol diet. Intestinal and hepatic HMG-CoA reductase activities and serum lipid profiles showed a trend toward compensation for dietary cholesterol deprivation but did not differ statistically between the cholesterol-fed versus -deprived groups. It is concluded that dietary cholesterol deprivation in the male neonatal pig causes alterations in growth, but no other statistically significant responses were detectable in this study.

Analysis of Variance↗
PubMed1991

Effect of ethanol on epidermal growth factor receptor in buccal mucosa.

The effect of ethanol on buccal mucosal epidermal growth factor receptors was investigated. The buccal mucosal cells from adult rats were incubated in DMEM at 4 degrees C and 37 degrees C in the presence of various concentrations (0-5%) of ethanol and then assayed for EGF receptor binding using [125I]-EGF. The results of binding analysis showed that the cells incubated in the presence of ethanol displayed diminished [125I]-EGF binding. The receptor binding capacity was dependent upon ethanol concentration and was more pronounced at 4 degrees C. A 30% decrease in receptor binding occurred with 1% ethanol, 34% with 2.5% ethanol, while 5% ethanol caused a 42% decrease in binding. Scatchard analysis suggested that the decrease of [125I]-EGF binding to the buccal mucosal cells pre-incubated with ethanol was due to a decrease of the high affinity binding site (Bmax). The association constant of the high affinity EGF receptor remained unchanged. The results suggest that ethanol due to its untoward effect on the receptor binding of salivary GF interferes with the process of epithelial renewal, thus leading to weakening of the mucosal defense perimeter of soft oral tissue and the onset of dysplasia.

Animals↗