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At least 19 recordsLinked to original sources
PubMed1994

Epidermal growth factor, transforming growth factor alpha, transforming growth factor beta, acidic fibroblast growth factor, basic fibroblast growth factor, and interleukin-1 proteins in the cornea.

The purpose of this study was to determine whether epidermal growth factor (EGF), EGF receptor, transforming growth factor alpha (TGF-alpha), transforming growth factor beta (TGF-beta), acidic fibroblast growth factor (acidic-FGF), basic fibroblast growth factor (basic-FGF), and interleukin-1-alpha (IL-1-alpha) proteins were present in cultures of human corneal cells and/or in sections of human corneal tissue. Immunohistochemistry was performed on human corneal sections. Immunofluorescent cell staining was used to evaluate corneal epithelial, stromal fibroblast, and endothelial cells in primary culture. Basic-FGF production was evaluated in culture cells using immunoprecipitation. EGF, TGF-alpha, TGF-beta-1, and IL-1-alpha were detected by immunohistochemistry in cells in all three layers of the cornea. EGF receptor and acidic FGF were detected by immunohistochemistry in epithelial and endothelial cells, but not in stromal fibroblast cells. Differences in distribution of the growth factors were noted within individual layers of the cornea. EGF and basic-FGF proteins were detected in all three predominant cell types of the cornea using immunocytology. IL-1-alpha protein was detected by immunocytology in corneal epithelial and endothelial cells, but not stromal fibroblasts. Immunoprecipitation confirmed the production of basic-FGF in all three cell types. IL-1-alpha protein detection in the corneal stroma by immunohistology, but not by immunocytology in first passage stromal fibroblasts, suggests that IL-1-alpha may localize to the corneal stroma after production by corneal epithelial and/or endothelial cells.

Adult↗
PubMed2000

Immunohistochemical localization of vascular endothelial growth factor, transforming growth factor alpha, and transforming growth factor beta1 in human corneas with neovascularization.

PURPOSE: To analyze presence and distribution of vascular endothelial growth factor (VEGF), transforming growth factor (TGF)alpha, and TGFbeta1 in human corneas with neovascularization due to different corneal diseases. METHODS: Indirect immunohistochemistry for VEGF, TGFalpha, and TGFbeta1, was performed on paraffin-embedded corneas obtained by keratoplasty. Corneas from each of the four main groups of histopathologic diagnoses associated with corneal neovascularization were analyzed (scarring after keratitis, graft rejection/insufficiency, acute necrotizing keratitis, scarring after mechanical/chemical injury). Subclassification of inflammatory infiltrates was done using immunohistochemistry for CD3 (T-lymphocytes) and CD68 (macrophages). RESULTS: The analyzed angiogenic factors were detectable in corneas from all four histopathologic groups in a similar distribution; capillary endothelial cells, stromal and intravascular inflammatory cells (T-lymphocytes, macrophages), and basal corneal epithelial cells stained positive for the tested angiogenic factors. CONCLUSION: The angiogenic factors VEGF, TGFalpha, and TGFbeta1 are detectable in human corneas with neovascularization. Their distribution is quite uniform in different corneal diseases, resulting in corneal angiogenesis. An antiangiogenic therapy inhibiting corneal neovascularization by antagonizing angiogenic factors would have to counteract several angiogenic factors.

Antigens, CD↗
PubMed1996

Expression of hepatocyte growth factor, transforming growth factor alpha, and transforming growth factor beta 1 messenger RNA in various human liver diseases and correlation with hepatocyte proliferation.

Hepatocyte growth factor (HGF) and transforming growth factor alpha (TGF-alpha) stimulate liver regeneration, whereas transforming growth factor beta 1 (TGF-beta 1) inhibits it in rats. However their significance in human liver diseases, especially in severe acute liver injury, remains unclear. We studied HGF, TGF-alpha, and TGF-beta 1 messenger RNA (mRNA) expression in the livers of patients with live diseases using a competitive reverse transcriptase polymerase chain reaction. As little as a twofold difference in mRNA expression could be detected from minute liver biopsy samples. We then examined cell proliferation using proliferating cell nuclear antigen (PCNA) staining. HGF mRNA levels were significantly higher (approximately threefold) in acute hepatitis (AH) than in exacerbation of chronic liver disease (EX) (P < .05). TGF-alpha mRNA levels were significantly greater in AH (approximately twofold) than EX (P < .05), and the levels were significantly higher (approximately threefold) in chronic hepatitis (CH) than in EX (P < .05). The TGF-beta 1 mRNA levels in all the groups were not significantly different. In acute liver injury (AH and EX), there was a significant correlation between HGF mRNA expression and the PCNA labeling index (LI) in the liver (r = .87, P < .005). TGF-alpha mRNA expression also correlated with the PCNA LI (r = .92,P < .0001). There was no significant correlation between the serum HGF and the PCNA LI in the liver. In conclusion, HGF and TGF-alpha produced in the liver stimulate hepatocyte proliferation in response to acute liver injury in humans.

Base Sequence↗
PubMed1997

Spatial and temporal patterns of expression of epidermal growth factor, transforming growth factor alpha and transforming growth factor beta 1-3 and their receptors in mouse jejunum after radiation treatment.

The goal of the present study was to assess changes in proliferation in the mouse jejunum after irradiation and the role of the growth factors EGF, TGF-alpha and TGF-beta 1-3 in the proliferative response. Our working hypothesis was that feedback signals from the villus to cells in the crypt regulate proliferation, and that the growth factors EGF and TGF-alpha with their common receptor EGF-R are involved in stimulation of proliferation, while the growth factors TGF-beta 1-3 with their receptors TGF-beta RI and TGF-beta RII are involved in inhibition of proliferation during this regulation. Immunohistochemical detection methods and automated image analysis were used for objective quantification of growth factor expression. The data indicate that, after 5 Gy irradiation, growth stimulation in the crypts takes place before major changes in the villi are observed. However, the combination of the reduction in the cell number, the number of cells expressing TGF-beta 1-3 and the reduction in the level of expression of TGF-beta 1-3 in the villi may cause the release of crypt cells from regulatory growth inhibition and initiate a proliferation-stimulating signal by an increase in the production of TGF-alpha and EGF. Regulation of proliferation after initiation of a proliferative response seems to be related more to the growth factors EGF, TGF-alpha and TGF-beta 3 in the crypts than to villus cellularity or growth factor expression, supporting the concept of stem cell autoregulation as a mechanism of cell regeneration in the intestinal crypt.

Animals↗
PubMed2002

Expression of growth factors and structural proteins in chordomas: basic fibroblast growth factor, transforming growth factor alpha, and fibronectin are correlated with recurrence.

OBJECTIVE: To test the hypothesis that the expression of certain growth factors and/or structural proteins is correlated with the biological behavior of cranial base chordomas. METHODS: The study investigated 14 pathological specimens of cranial base chordomas from patients who were monitored for at least 2 years after their initial operations. Some cases involved multiple tumor recurrences and multiple operations. For those patients, the time to recurrence after each operation was recorded and a mean value was calculated. Nine patients with mean times to recurrence of 24 months or more or with 24 months of follow-up monitoring without recurrence after single operations were designated the "good-prognosis" group. Five patients with mean times to recurrence of less than 24 months were designated the "poor-prognosis" group. In each case, only the specimen from the initial operation was studied. Multiple sequential sections were cut from paraffin-embedded blocks of tissue and immunohistochemically prepared for detection of three growth factors and three structural proteins, i.e., basic fibroblast growth factor, transforming growth factor alpha, vascular endothelial growth factor, fibronectin, collagen III, and collagen IV. Intensity of expression was graded by using a four-tier system (Grades 0, 1, 2, and 3). Levels of expression of the molecules in the two groups were evaluated and compared. RESULTS: The mean transforming growth factor alpha expression intensity grades for the good- and poor-prognosis groups were 0.8 and 2.6, respectively, and the corresponding mean basic fibroblast growth factor grades were 1.4 and 2.6. For both groups, the mean grade for vascular endothelial growth factor expression was 0.6. For fibronectin, the mean staining grades for the good- and poor-prognosis groups were 2.2 and 3.0, respectively. The corresponding mean intensities for collagen III were 1.1 and 0.8, and those for collagen IV were 2.5 and 2.6. CONCLUSION: Our descriptive data from immunohistochemical analyses of chordomas suggest that high levels of transforming growth factor alpha and basic fibroblast growth factor expression are linked to higher rates of recurrence. Strong fibronectin expression may also be a marker of aggressive biological behavior.

Chordoma↗
PubMed1992

The effects of epidermal growth factor, transforming growth factors alpha and beta and platelet-derived growth factor on murine palatal shelves in organ culture.

Palatal shelves isolated from day-13 embryonic mice were explanted on to the surfaces of collagen gels either singly or in pairs with their medial edges in contact, and cultured submerged in a 1:1 mixture of Dulbecco's modified Eagle's medium/Ham's F12 medium. The medium was supplemented with either 10 ng/ml epidermal growth factor (EGF), 10 ng/ml transforming growth factor alpha (TGF alpha), 1 ng/ml transforming growth factor beta (TGF beta 1) or 2 ng/ml platelet-derived growth factor (PDGF) all in the presence or absence of 2.5% donor calf serum (DCS). Cultures were terminated after 0, 24, 48 or 72 h and processed for histological and immunocytochemical examination. In serum-free medium and medium supplemented with 2.5% DCS the palatal epithelia differentiated in a manner similar to that seen in vivo (oral, keratinization; nasal, pseudostratified, ciliated columnar cells and medial edge, epithelial degeneration). A similar pattern was obtained in serum-free medium supplemented with either EGF or TGF alpha. However in cultures with either EGF or TGF alpha plus 2.5% DCS present in the medium, medial-edge epithelial degeneration was inhibited and the oral epithelia were more heavily keratinized. The mesenchyme of such cultures stained more intensely for various extracellular matrix molecules. In TGF beta 1-supplemented cultures (with, but especially without, serum supplementation) the epithelia were thin, medial-edge epithelial degeneration was marked, and the fibronectin content of the mesenchyme was increased. PDGF prevented medial-edge epithelial degeneration in the presence, but not in the absence, of serum; mesenchymal extracellular molecules were not as prevalent as with the EGF treatment. These results indicate that exogenous growth factors (including those present in serum) exert effects on organ-cultured mouse palatal shelves in a fashion similar to their effects in cell culture and that controlled physiological levels of such factors may be important in mouse palatal development.

Animals↗
PubMed1999

The genome of cowpox virus contains a gene related to those encoding the epidermal growth factor, transforming growth factor alpha and vaccinia growth factor.

Cowpox virus (CPV) is a member of the Orthopoxvirus genus and has the genetic capacity to encode a multitude of genes that interfere with the host inflammatory and immune response or modulate the physiological state of infected and non-infected cells. Among these CPV factors are receptors homologous to interferon and tumor necrosis factor receptors and also a viral cellular serine-proteinase analog. Here we describe the detection of a CPV gene that encodes a protein homologous to epidermal growth factor, transforming growth factor alpha and poxvirus growth factors, such as the vaccinia growth factor (VGF). The VGF and other poxvirus growth factors are produced early in the infection and are secreted into the medium where they bind to the EGF receptors, generating mytotic responses. The cowpox growth factor (CGF) gene was detected in three copies on the virus genome by PCR, and by northern and southern blot hybridization using VGF nucleotide sequences as primers and probes. The CPV gene has a strong nucleotide and predicted amino acid similarity with VGF, and is also produced early in the infection.

Amino Acid Sequence↗
PubMed2000

[Electron-immunostaining characteristics of platelet-derived growth factor, transforming growth factor beta1 and their receptors in epiretinal membranes].

OBJECTIVE: To investigate the ultrastructural distribution of platelet-derived growth factor (PDGF), transforming growth factor beta(1) (TGF-beta(1)) and their receptors in epiretinal membranes (ERM) and discuss the clinical significance of the distribution. METHODS: 25 membrane specimens were surgically removed by vitrectomy from 9 patients with rhegmatogenous retinal detachment. Double-staining techniques of immunoelectromicroscopy for eight antibodies (PDGF, TGF-beta(1), PDGF receptor subunits alpha and beta, TGF-beta subunits I and II, type I and III collagen) were used in these specimens as previously designed. RESULTS: PDGF and TGF-beta(1) staining appeared to be stronger on early (< 2 months) and late (> 6 months) stage membranes than that of middle (2 - 6 months) stage of membranes, and the immunostaining intensity inverted with the degree of proliferative vitreoretinopathy (PVR). We found that the gold particles of PDGF and TGF-beta(1) tended to get together with that of type I and III collagen. In addition, the stainings of four growth factor receptors were frequently positive in a type of epithelial-like cells with rich cytoplasm components, and also the gold particles of PDGF and TGF-beta(1) were found around these cells. CONCLUSIONS: A concentration change of PDGF and TGF-beta(1) exists in development of ERM throughout. The epithelial-like cells are of a type of active cells, and autocrine and paracrine activity may be involved in ERM pathogenesis. PDGF and TGF-beta(1) influence the contractile activity of ERM.

Epiretinal Membrane↗
PubMed1994

Immunoreactivity of antibodies to epidermal growth factor, transforming growth factors alpha and beta, and epidermal growth factor receptor in the premenopausal ovary.

This study provides a valuable insight into the localization of growth factors in paraffin sections of human ovarian tissue. Antibodies to epidermal growth factor (EGF), transforming growth factors alpha and beta (TGF alpha and beta) and epidermal growth factor receptor (EGFR) were applied to paraffin sections of 16 cases of formalin-fixed normal or benignly abnormal ovarian tissue. All growth factor antibodies reacted with theca, but not granulosa cells, whilst the antibody to EGFR reacted with both types of follicular cells and was weakly reactive in ovarian stroma. There were no discernible qualitative changes in reactivity during the follicular cycle. These immunohistochemical findings generally support previously published molecular and biochemical data from tissue culture. One exception is in the observation of immunoreactivity to EGF in theca and granulosa cells. This may be due to differences in sensitivity of the methods in use. The possibility of a cross-reaction of the anti-EGF antibody with TGF alpha is also discussed. This study provides evidence for both paracrine and autocrine roles for growth factors in folliculogenesis.

Adult↗
PubMed1993

Regulation of inhibin secretion in human placental cell culture by epidermal growth factor, transforming growth factors, and activin.

In this study, the effects of epidermal growth factor (EGF), transforming growth factor-alpha (TGF alpha), TGF beta 1, and activin-A on inhibin secretion were investigated in primary culture of human placental cells. Immunoreactive inhibin in the culture medium was measured by immunoenzymatic assay. EGF stimulated testosterone-induced inhibin secretion in placental cells. Although testosterone alone induced only a slight enhancement of inhibin release in the culture, treatment of trophoblast cells with EGF and testosterone caused a significant increase in inhibin secretion, with immunoreactive inhibin levels much higher than those of testosterone or EGF alone. TGF alpha combined with human placental lactogen (hPL) had a stimulatory effect on inhibin secretion in placental cell culture. Simple addition of either TGF alpha or hPL to the culture did not show any effect on inhibin secretion in placental cells. A remarkable augmentation of inhibin secretion was obtained after the trophoblasts were exposed to both TGF alpha and hPL simultaneously. TGF beta 1 and activin-A showed synergistic effects to suppress inhibin secretion in placental cells. TGF beta 1 alone did not show any action on inhibin secretion, and activin-A alone induced a small decrease in inhibin release in the culture. In the presence of activin-A, addition of TGF beta 1 to the culture induced a profound decrease in immunoreactive inhibin levels in the medium. Activin-A could also suppress hCG-induced inhibin secretion in placental cells. Addition of hCG alone resulted in a small, but not significant, increase in inhibin release in the cultured cells, whereas the presence of activin-A combined with hCG in the culture conversely decreased inhibin secretion in the culture, with immunoreactive inhibin levels significantly lower than those in the presence of hCG or activin-A alone. These findings suggest that EGF and TGF alpha, alone or in combination with other hormones, may be stimulators, and TGF beta and activin may act as suppressors of inhibin secretion in human placental cells.

Activins↗
PubMed1984

Differential effects of epidermal growth factor, transforming growth factor, and insulin on DNA and protein synthesis and morphology in serum-free cultures of AKR-2B cells.

The effects of epidermal growth factor (EGF), insulin, and a transforming growth factor from fetal bovine serum on protein synthesis, DNA synthesis, and morphology in confluent cultures of AKR-2B mouse cells have been examined. The cells were plated and grown to confluence in serum-containing medium, and then the medium was changed to MCDB 402 containing no undefined supplements for 2 days before the addition of the polypeptides to be tested. Under these conditions, all of the factors listed above stimulated rapid increases in protein synthesis. When added to cultures singly, however, only EGF stimulated significant DNA synthesis. The effect of EGF on DNA synthesis was highly synergistic with insulin. Fetal serum transforming growth factor activity, which stimulated multiple rounds of cell replication in soft agar in serum-containing medium, did not stimulate DNA synthesis in serum-free monolayer cultures of these cells when added alone or in combination with EGF or insulin. Fetal serum transforming growth factor did, however, stimulate a rapid change in the morphology of these cells from flat, nonoverlapping cells to bipolar, multilayered cultures when added to the serum-free medium.

Animals↗
PubMed1991

Epidermal growth factor and its receptor, basic fibroblast growth factor, transforming growth factor beta-1, and interleukin-1 alpha messenger RNA production in human corneal endothelial cells.

The authors tried to determine whether human corneal endothelial cells in primary culture synthesize messenger RNA (mRNA) coding for epidermal growth factor (EGF), EGF receptor, basic fibroblast growth factor (FGFb), transforming growth factor beta-1 (TGFb1), and interleukin-1 alpha (IL-1 alpha). Oligodeoxythymidine-primed complementary DNA (cDNA) was generated from total cellular RNA extracted from eight independent primary corneal endothelial cell cultures. Four of these cultures, maintained 18-51 days, had obvious increases in cell numbers and mass over the 2 weeks before RNA extraction and were populated primarily with cells that were small, uniform, and mononuclear (proliferative cultures). The morphology of the cells in other four cultures, maintained 47-78 days, was predominantly large, irregular, vacuolated, and occasionally multinucleated. These cells were identical to senescent cells found in previous studies, and the cell number did not increase in these cultures over the 2 weeks preceding RNA extraction (senescent cultures). The polymerase chain reaction (PCR) was used to amplify the growth factors (EGF, FGFb, TGFb1, and IL-1 alpha), EGF receptor, and beta actin sequences from each of the cDNA samples. The EGF receptor, FGFb, and beta actin mRNAs were present in all eight cDNA samples. The EGF mRNAs were detected by PCR alone in four of the samples from proliferative cultures, TGFb1 mRNAs in three, and IL-1 alpha mRNAs in three. In the samples from senescent cultures, 0, 1, and 0 mRNAs were detected, respectively. Southern blots of the PCR products were probed with oligonucleotides complementary to sequences in each of the amplified products. This technique showed that the appropriately sized amplification products were specific.(ABSTRACT TRUNCATED AT 250 WORDS)

Actins↗
PubMed1994

Retinal and preretinal localisation of epidermal growth factor, transforming growth factor alpha, and their receptor in proliferative diabetic retinopathy.

A number of growth factors have been implicated in the development and perpetuation of preretinal fibrovascular membranes in patients with proliferative diabetic retinopathy (PDR). The aim of this study was to determine the potential role of epidermal growth factor (EGF), transforming growth factor alpha (TGF-alpha), and their receptor (EGF-R) in PDR development. Immunostaining for EGF, TGF-alpha, and EGF-R was compared between normal retina, PDR retina, and PDR preretinal membranes. Weak staining for EGF and EGF-R was observed throughout the neural retina from non-diabetic eyes while weak to moderate staining for TGF-alpha was observed in the ganglion cell layer and the inner and outer nuclear layers. In contrast, intense staining for EGF and TGF-alpha and moderate staining for EGF-R were observed throughout the PDR retina. Immunoreactivity for EGF, TGF-alpha, and EGF-R was seen in the majority of the 11 excised membranes studied and, though variable, was generally greater than that observed in normal retinas. These results suggest an autocrine/paracrine role for EGF, TGF-alpha, and EGF-R in PDR.

Diabetic Retinopathy↗
PubMed1994

Effect of epidermal growth factor, transforming growth factor alpha and nerve growth factor on gastric mucosal integrity and microcirculation in the rat.

In the present study we have compared the effects of the peptide growth factors epidermal growth factor (EGF), transforming growth factor alpha (TGF alpha) and nerve growth factor (NGF) on gastric mucosal integrity and mucosal blood flow in the rat. Mucosal damage was assessed 30 min after intraluminal instillation of 40% (w/v) ethanol (EtOH). EtOH treatment resulted in an increase in mucosal damage when compared to saline treated control animals. Administration of each growth factor either by tail vein (i.v.; 0.2-1 nmol/kg) or via the left gastric artery (i.a.; 0.05-0.2 nmol/kg) resulted in a significant reduction in the extent of mucosal damage. The growth factors reduced EtOH-mediated damage in an equipotent manner. The reduction in the area hemorrhagic damage ranged from -25 to -35% from EtOH alone when the factors were administered i.a. and from -75 to -85% when delivered i.v. Gastric mucosal blood flow as assessed by laser Doppler flowmetry (LDF) was increased in a dose-dependent and equipotent manner by EGF and TGF alpha administered either by the i.v. or i.a. route. LDF changes were greater when EGF or TGF alpha were delivered via the i.a. route. NGF did not significantly increase blood flow regardless of the dose or route of delivery. beta-Adrenoceptor blockade with propranolol (0.75 mg/kg i.v.) abolished the increase in LDF in response to EGF or TGF alpha but did not affect the ability of these growth factors to reduce EtOH-mediated damage.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

The effect of epidermal growth factor, transforming growth factor and breast tumour homogenates on the activity of oestradiol 17 beta hydroxysteroid dehydrogenase in cultured adipose tissue.

The effect of epidermal growth factor (EGF), transforming growth factor (TGF alpha) and breast tumour homogenates on oestradiol 17 beta hydroxysteroid dehydrogenase (E2DH) activity has been examined using cultured human breast adipose tissue. EGF (100-1000 ng/ml) inhibited E2DH activity (E1----E2) in a dose dependent manner. TGF alpha (250 and 500 ng/ml) stimulated E2DH activity, with conversion of E1----E2 increasing to a greater degree than E2----E1 activity. Breast tumour homogenates (2-10% w/v) also influenced E2DH activity. It is concluded that growth factors, produced by breast tumours, may modulate E2DH activity in tissues surrounding the tumour and thereby influence tumour growth.

17-Hydroxysteroid Dehydrogenases↗
PubMed1992

Mitotic responsiveness of cultured adult human hepatocytes to epidermal growth factor, transforming growth factor alpha, and human serum.

The present study was undertaken to evaluate the ability of human hepatocytes to respond in culture to various mitotic agents including epidermal growth factor (EGF), transforming growth factor alpha (TGF-alpha), or serum from patients with fulminant hepatitis. Human hepatocytes were maintained in culture on collagen-coated plates in a chemically and hormonally defined serum-free medium at low cell density. Twelve hours after plating, cultures were treated with increasing amounts of EGF (1-100 ng/mL), TGF-alpha (1-100 ng/mL), or human serum (1%-10%) for 0-96 hours. Proliferative response was assessed by determining against time the rate of DNA synthesis by [3H]thymidine incorporation in DNA, the labeling index, the expression of cyclin A, the amount of DNA, and the number of cells. The rate of DNA synthesis reached a maximum after 48 hours of treatment with 20 ng/mL EGF, 40 ng/mL TGF-alpha, or 5%-10% of human serum (fulminant hepatitis); the average increase with respect to untreated cells was 4.35 times with EGF, 5.4 times with TGF-alpha, and 4-6 times with serum from patients with fulminant hepatitis. The maximum expression of cyclin A coincided with the maximum of DNA synthesis. After 72 hours of treatment with EGF or human serum (fulminant hepatitis), the amount of DNA increased by 75%-100% (P less than 0.001) and the number of cells by 50% (P less than 0.001). These results show that adult human hepatocytes respond to mitogens, as expected from previous studies on animal hepatocytes, and provide experimental basis for future investigations in the field of human liver regeneration.

Adult↗
PubMed1996

Immunohistochemical localization of the epidermal growth factor, transforming growth factor alpha, and their receptor in the human mesonephros and metanephros.

The distribution of epidermal growth factor (EGF), transforming growth factor alpha (TGF alpha), and EGF/TGF alpha receptor were studied by means of immunohistochemical methods starting from the very early stages of human embryonic kidney development. Mesonephros and metanephros were examined in order to detect immunoreactive staining in serial sectioned embryos and fetal kidneys. Anti-EGF immunoprecipitates were found in the S-shaped mesonephric vesicles of 6-week old embryos as well as in the mesonephric duct albeit with a lower degree of reactivity. Intense reactivity was observed in the metanephros within the blastemic caps of the same gestational period; the reaction was weaker within the ureteric bud branches. Bowman's capsule, proximal tubules, and collecting ducts were also reactive in the fetal kidney to varying degrees. The distribution of TGF alpha reactivity in the mesonephros was similar to that observed for EGF but with a lower intensity. In contrast, there was no reactivity in the metanephros, at least during the embyronic periods examined. By the 11th week of gestation, an intense reactivity for TGF alpha polipeptide was shown in the fetal kidney at the level of the proximal tubules and Bowman's capsule; distal tubules as well as all urinary structures from the collecting ducts to the pelvis were less reactive. Finally, EGF/TGF alpha receptor reactivity was identified by the 6th week of development, being more intense in the mesonephros at the level of the mesonephric duct cells. In the metanephros, the ureteric bud-derived branches were reactive, whereas most of the blastemic tissue did not stain. By the 11th week, only the collecting ducts and the remaining urinary structures contained reaction products: Reactivity was distributed to the tissues originating from the ureteric bud branching. Taking into account recent advances in knowledge about the biology of growth factors, the hypothesis is proposed that the secretory components (vesicles, glomerulus, and tubules) of renal anlagen might release the growth factors while the cells of the urinary tract (i.e., collecting duct, pelvis, etc.) may be their targets.

Epidermal Growth Factor↗
PubMed1993

Expression of epidermal growth factor, transforming growth factor alpha and their receptor in gastro-oesophageal diseases.

This article is a review of aspects of the expression of the regulatory peptides; epidermal growth factor (EGF), transforming growth factor alpha (TGF-alpha), and their receptor (EGF-R) in the epithelium of the human oesophagus and stomach in health and disease. It has become clear that TGF-alpha has increased expression in metaplastic, dysplastic and neoplastic tissue of the oesophagus compared with normal mucosa. The degree of abnormal expression becomes more marked as dysplasia increases. TGF-alpha expression is also increased in gastric neoplasias. EGF has a different pattern of expression, being decreased in oesophagitis and increased in gastritis. Although EGF is present in Barrett's oesophagitis, the expression of EGF does not discriminate between dysplastic and neoplastic epithelium. EGF-R is normally expressed on all gastro-intestinal epithelia, but its expression is increased in Barrett's epithelium, as well as in adenocarcinomas of the oesophagus and the stomach. The two peptides bind to their receptors on the mucosal cell membranes, and the co-expression of peptide and receptor is positively associated with varying degrees of cellular proliferation. The density of receptor expression may modulate the proliferative stimulus, leading to either mitogenic (regulated) or oncogenic (unregulated) growth.

Epidermal Growth Factor↗