epidermal-growth-factor and Edema

Angiogenesis, the development of new vessels from a pre-existing vasculature, accompanies the growth and malignant transformation of astrocytic brain tumors. Neovascularization is essential for sustained tumor growth, and with increasing grade, astrocytic tumors undergo an, angiogenic switch, manifested by marked increases in vessel density and changes in vascular morphology. In the quiescent state, endogenous anti-angiogenic factors including endostatin, thrombospondin, and soluble vascular endothelial growth factor receptor-1 (sVEGFR-1) balance the actions of pro-angiogenic stimuli and restrain the angiogenic switch. Once activated, pro-angiogenic factors including most notably basic fibroblast growth factor (FGF), vascular endothelial growth factor (VEGF-A), and platelet-derived growth factor (PDGF) incite robust astrocytoma neovascularization. Recent studies have also explored the expression patterns and functional importance of the angiopoietins, Tie2 and neuropilin receptors, and hepatocyte growth factor/scatter factor (HGF). Together these angiogenic factors have diverse actions on endothelium and perivascular supporting cells that engender tumor neovessels with a unique phenotype, distinct from normal vessels. Properties of the astrocytoma neovasculature contribute to tumor growth, malignant progression, invasion, hemorrhage, and edema formation. Thus, the mechanistic actions of angiogenic factors on cerebral microvessels and the nature of the resultant tumor neovasculature establish a framework for understanding many of the characteristic behaviors of astrocytoma tumors.

Topics: Angiopoietins; Animals; Astrocytes; Astrocytoma; Brain; Brain Neoplasms; Disease Progression; Edema; Epidermal Growth Factor; Fibroblast Growth Factor 2; Hepatocyte Growth Factor; Humans; Neovascularization, Pathologic; Neuropilins; Platelet-Derived Growth Factor; Vascular Endothelial Growth Factor A; Vascular Endothelial Growth Factor Receptor-1

Patients who receive laser treatments may experience transient erythema, edema, and crusts for several days. Although a variety of growth factor-containing creams for promoting recovery after laser treatment are available, evidence for their efficacy remains insufficient.. We performed a randomized controlled split-face study to assess the effects of a multigrowth factor (MGF)-containing cream on patients recovering from laser treatment.. Twenty patients underwent treatment using an ablative fractional laser and were randomized with respect to the side of the face treated with an MGF-containing cream or control cream. We measured post-treatment erythema and pigmentation using the erythema and melanin indices, respectively, and evaluated the total area of microcrusts with dermoscopy. Additionally, patient satisfaction levels and global improvement scores were assessed.. We found that the area of microcrusts was significantly smaller in the MGF-treated regions. Global improvement scores for post-treatment edema and wrinkles were also significantly higher for MGF cream-treated sides than for the control sides.. The MGF cream-treated regions showed a more rapid recovery from crusts and edema. Thus, the use of an MGF-containing cream after laser treatment can effectively reduce recovery time.

Topics: Adult; Cosmetic Techniques; Dermoscopy; Double-Blind Method; Drug Combinations; Edema; Epidermal Growth Factor; Erythema; Face; Female; Fibroblast Growth Factors; Humans; Intercellular Signaling Peptides and Proteins; Lasers, Gas; Male; Middle Aged; Patient Satisfaction; Photography; Pigmentation Disorders; Platelet-Derived Growth Factor; Prospective Studies; Skin Aging; Skin Cream; Vascular Endothelial Growth Factor A; Wound Healing; Young Adult

Epidermal growth factor (EGF) and its receptor (EGF-R) are attractive targets for cancer immunotherapy. Tolerance has been broken with an EGF-vaccine and antibodies against EGF have been produced in animals and in cancer patients. EGF also plays an important role in the inflammation stage of wound healing. Because this therapeutic approach may be of importance after surgery procedures in cancer patients, we decided to investigate the possible role of the EGF-vaccine in the croton-oil-induced ear edema and in the wound healing experimental animal models.. Mice were immunized with an EGF-vaccine by intramuscular injections and serum titers against EGF were measured through ELISA techniques. Control animals received saline.. Immunized mice produced antibodies against EGF while no antibody titers could be measured in control animals. Croton oil applied to the inner ear surface of EGF-vaccine treated mice caused a 61.3% lower ear punch weight and a 60.2% lower myeloperoxidase activity than control mice. In the EGF-vaccine treated animals, planimetry measurements and histological analysis did not led to significant impairment in tissue repair.. The EGF-vaccination in mice decreased the normal croton-oil-induced inflammation response, without apparent impairment in tissue healing.

Topics: Animals; Antibody Formation; Autoantibodies; Cancer Vaccines; Croton Oil; Dermatologic Agents; Drug Combinations; Ear Diseases; Edema; Epidermal Growth Factor; Image Processing, Computer-Assisted; Immunization; Inflammation; Injections, Intramuscular; Mice; Mice, Inbred BALB C; Skin; Wound Healing; Wounds, Penetrating

In order to get further evidence for a mandatory involvement of epidermal growth factor (EGF) in the neutrophic action of vitamin B12 (cobalamin (Cbl)) in the central nervous system (CNS) of the rat, we observed the effects of repeated intracerebroventricular (ICV) microinjections of EGF in rats made Cbl-deficient through total gastrectomy. Morphometric analysis demonstrated a significant reduction in both intramyelinic and interstitial edema in the white matter of the spinal cord (SC) of totally gastrectomized (TGX) rats after treatment. Intramyelinic and interstitial edema are characteristic of Cbl-deficient central neuropathy in the rat. Similar lesions were also present in SC white matter of rats treated with repeated ICV microinjections of specific anti-EGF antibodies without any modification in their Cbl status. These results, together with those of a previous study showing the cessation of EGF synthesis in the CNS of TGX rats, demonstrate that: a) EGF is necessarily involved in the signaling pathway of Cbl in the rat CNS; and b) the lack of a neurotrophic growth factor EGF, and not the mere withdrawal of Cbl, causes or at least contributes to neurodegenerative Cbl-deficient central neuropathy.

Topics: Animals; Antibodies, Monoclonal; Cerebral Ventricles; Edema; Epidermal Growth Factor; Gastrectomy; Humans; Injections, Intraventricular; Male; Nerve Fibers, Myelinated; Rats; Rats, Sprague-Dawley; Signal Transduction; Spinal Cord; Vitamin B 12; Vitamin B 12 Deficiency

The effect of subcutaneous and luminal epidermal growth factor (EGF) administration on acetic acid-induced colonic ulceration was determined in adult rats. Application of acetic acid to the distal colonic lumen caused epithelial denudation, mucosal ulceration and inflammation in the exposed segment. Re-epithelialization was detectable 5 to 7 days later, with near-complete resolution of the lesion by 14 days post-injury. Luminal EGF (1.6 mg/kg bw/day) or subcutaneous EGF (200 micromilligrams/kg bw/day), administered for 4 or 6 days from the time of ulceration failed to enhance re-epithelialization of the acid-exposed segment. However, mucosal and submucosal thickening was attenuated 20-40% by subcutaneous EGF, reflecting a reduction in edema. Luminal EGF had a similar but less substantial effect in the submucosa, but was more effective at attenuating muscularis thickening adjacent to the lesion. In conclusion, administration of exogenous EGF for up to 6 days failed to enhance re-epithelialization of acetic acid-induced colonic ulcerations but did attenuate the associated edematous response.

Topics: Acetic Acid; Animals; Cell Division; Colon; Colonic Diseases; Edema; Epidermal Growth Factor; Epithelium; Histocytochemistry; Intestinal Mucosa; Male; Proliferating Cell Nuclear Antigen; Rats; Rats, Sprague-Dawley; Ulcer