Disease relevance of EGF

• Transforming growth factor-alpha (TGF-alpha) and vaccinia growth factor (VGF) have substantial sequence homology with EGF, and all appear to bind to the same receptor protein [1].
• There is a good correlation between levels of decline in EGF binding and loss of body weight among TCDD-treated rats [2].
• TCDD causes a significant reduction in EGF binding at an early stage of toxicity (day 2) and at very low doses (1 microgram/kg, single i.p., rat) [2].
• In this study, to investigate the substrate specificities of tyrosine kinases, we have examined the actions of the purified epidermal growth factor (EGF) receptor kinase and Rous sarcoma virus src kinase on purified microfilament- and microtubule-related proteins [3].
• In addition, the ULF factor stimulates DNA synthesis in human A431 epidermoid carcinoma cells, whereas EGF is inhibitory [4].

High impact information on EGF

• Epidermal growth factor (EGF) stimulates the proliferation of keratinocytes in culture, and topical administration of EGF accelerates epidermal regeneration of partial thickness burns or split-thickness incisions in vivo [1].
• Epidermal growth factor is known to stimulate growth of keratinocytes in vitro, thus it might be expected to promote wound healing [5].
• Germ-free conditions and antiserum against Clostridium perfringens toxin prevented intestinal dysfunction and NEC in formula-fed pigs, whereas the gut trophic factors, epidermal growth factor, and glucagon-like peptide 2 had limited effects [6].
• CONCLUSIONS: EGF stimulates pepsinogen secretion by activating eicosanoid generation, tyrosine kinases, MAP kinases, Ca2+, NO, and guanosine 3',5'-cyclic monophosphate [7].
• EGF caused a concentration-dependent stimulation of pepsinogen secretion and MAP kinase activity and determined a 2.5-7.0-fold increase in [Ca2+]i, inositol 1,4,5-tryphosphate, prostaglandin E2, and leukotriene B4 [7].

Chemical compound and disease context of EGF

• During exposure to luminal acid, ex-EGF not only prevented intracellular acidosis but also promoted restitution [8].
• METHODS: Twenty-four minipigs with surgically induced portal hypertension underwent four consecutive weekly sessions of oesophageal sclerotherapy with 5 ml 1% polidocanol and were concomitantly treated with either a placebo or human recombinant EGF administered subcutaneously [9].
• Expression of enhanced green fluorescent protein (EGFP) and neomycin resistant (Neo(R)) genes in porcine embryos following nuclear transfer with porcine fetal fibroblasts transfected by retrovirus vector [10].

Biological context of EGF

• These findings show that EGF mRNA expression is temporally regulated during the cycle and early pregnancy, and this pattern of gene expression may be important during early conceptus development [11].
• A decrease in the intensity of EGF immunostaining was observed in the late luteal phase [12].
• The aim of our study was to determine EGF and EGFR immunoexpression in the uterine artery and its branches during the estrous cycle in the pig [12].
• The highest intensity of EGF and EGFR immunoreaction in endothelial cells of the uterine artery was observed in the follicular phase [12].
• Epidermal growth factor (EGF) and its receptor (EGFR) are expressed in many tissues, including reproductive organs, and is involved in angiogenesis, embryo implantation and development as well as in proliferation and differentiation of various cells [12].

Anatomical context of EGF

• Light microscopic observations revealed the phase-related immunoreactivity of EGF and EGFR in the endothelial cells of the uterine artery and its branches [12].
• In the endothelium of the uterine arterial branches, a significant increase in the intensity of EGF and EGFR-immunoreactivity was observed in the middle luteal phase [12].
• These results indicate that EGF acts directly upon cells within the gastric mucosa, and is most effective when applied to the serosal gastric surface [13].
• They further suggest that in vitro preparations of intact gastric mucosa can be used for analyzing the inhibitory effects of EGF on gastric acid secretion [13].
• BACKGROUND & AIMS: Although epidermal growth factor (EGF) inhibits gastric acid secretion, the effects it exerts on gastric chief cells are unknown [7].

Associations of EGF with chemical compounds

• Tyrosine kinase inhibitors and cyclooxygenase and lipoxygenase inhibitors reduced pepsinogen secretion and eicosanoid generation induced by EGF [7].
• Cyclic adenosine monophosphate-induced secretion was also reduced by EGF, although the effect occurred more slowly than in histamine-treated tissues [13].
• When applied to the luminal (mucosal) gastric surface, EGF inhibited secretion marginally but only at micromolar concentrations [13].
• The effect of in vivo-administered 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on epidermal growth factor (EGF) receptor activity of the rat hepatic plasma membrane was studied [2].
• Epidermal growth factor (EGF) increased EET production in F87V BM-3 cells, which was completely abolished by pretreatment with either 17-ODYA or the phospholipase A2 (PLA2) inhibitor, quinacrine [14].

Physical interactions of EGF

• Thus, the ability of porcine GCs to bind EGF was changed with differentiation in vivo, while both EGF-binding capacity and mitotic responsiveness were regulated by exposure to FSH in vitro [15].

Enzymatic interactions of EGF

• The EGF receptor in Day 13 conceptus membranes is a 170-kDa protein and was phosphorylated in the presence of EGF and adenosine triphosphate [16].

Regulatory relationships of EGF

• TGHQ, H(2)O(2), and EGF induce different EGFR tyrosine phosphorylation profiles that likely influence the subsequent differential kinetics of MAPK activation [17].
• These data show that TGF-alpha inhibits gastric acid secretion in a manner similar to EGF and that the two growth factors share at least one physiological action unrelated to their mitogenic properties [18].
• EGF-stimulated [3H]thymidine incorporation was reduced by TGF-beta 1 at concentrations above 0.1 ng/ml [19].
• FSH also regulated the mitotic responsiveness to EGF [15].
• Pretreatment of granulosa cells for 24 h with PMA abrogated the EGF-induced stimulation of follistatin mRNA accumulation [20].

Other interactions of EGF

• A significant decrease in the intensity of EGF and EGFR immunoreactivity was found in the middle luteal phase [12].
• The epidermal growth factor (EGF) gene, on porcine chromosome 8, may influence uterine capacity because of its growth-promoting activities [11].
• Photoreceptor survival correlated directly with increasing concentrations of FGF2, and also of EGF [21].
• To evaluate FSH and EGF effects on the endogenous StAR gene, chromatin immunoprecipitation assays were performed in combination with real-time polymerase chain reaction [22].
• Mapping of the porcine AREG and EGF genes to SSC8 [23].

Analytical, diagnostic and therapeutic context of EGF

• Intermediate responses were seen after treatment with 0.1 ng/ml of EGF [19].
• Western blot analysis of phosphotyrosine residues was used to monitor activation of FGF2 and EGF signaling pathways [21].
• Autoradiography of [3H]thymidine incorporation in EGF-treated cultures showed that more than 80% of nuclei in mother follicles and migrating cells were labeled after 4 days [24].
• On the other hand, EGF does not increase the rate of wound healing in this model even at 1000-fold higher doses than those used in in vitro bioassays [25].
• Cellular microinjection of anti-Crk-II antibody inhibited EGF-induced, but not insulin-induced, DNA synthesis [26].

References