Impact of Kuntai Capsules on LIF, IGF-1 and EGF expression in the implantation window of endometrium in mice / Impacto de cápsulas de Kuntai en la expresión de LIF, IGF-1 y EGF en la ventana de implantación de endometrio en ratones

To investigate the influence of Kuntai capsules on the expression level of leukemia inhibitory factor (LIF), insulin-like growth factor-I (IGF-1)and epidermal growth factor (EGF) during the mouse's implantation window of superovulation period and controlled ovarian hyperstimulation period. 90 female mice were randomly divided into six groups in control, superovulation and controlled ovarian hyperstimulation (COH) conditions. The RNA expression of EGF, LIF and IGF-1 in the endometrium on the 4th day of pregnancy was detected, and the relative expression was compared. mRNA expression of these three factors in endometrium was significantly lower in superovulation and COH groups than control group (p<0.001). mRNA expression of these three factors in endometrium remained obviously lower in superovulation plus kuntai capsule group and COH plus kuntai capsule group than control group (p<0.01). mRNA expression of these three factors in endometrium was lower in control group than in the NS plus kuntai capsule group (p<0.05). Kuntai capsule cannot completely reverse the endometrial damages caused by superovulation and COH. Thus Kuntai capsule could partially improve a mouse's endometrial receptivity during the implantation window.

Para investigar la influencia de las cápsulas de Kuntai en el nivel de expresión del factor inhibidor de la leucemia (LIF), el factor de crecimiento similar a la insulina I (IGF-1) y el factor de crecimiento epidérmico (EGF) durante la ventana de implantación del ratón del período de superovulación y la hiperestimulación ovárica controlada período, se dividieron aleatoriamente 90 ratones hembra en seis grupos en condiciones de control, superovulación e hiperestimulación ovárica controlada (COH). Se detectó la expresión de ARN de EGF, LIF e IGF-1en el endometrio al cuarto día de embarazo, y se comparó la expresión relativa. La expresión de ARNm de estos tres factores en el endometrio fue significativamente menor en los grupos de superovulación y COH que en el grupo control (p<0,001). La expresión de ARNm de estos tres factores en el endometrio permaneció más baja en el grupo de cápsulas de superovulación más Kuntai y en el grupo de cápsulas de COH más Kuntai respecto del grupo control (p<0,01). La expresión de ARNm de estos tres factores en el endometrio fue menor en el grupo control que en el grupo de cápsula NS más Kuntai (p<0,05). La cápsula de Kuntai no pudo revertir completamente los daños endometriales causados por la superovulación y la COH. Por lo tanto, se sugiere que la cápsula de Kuntai podría mejorar parcialmente la receptividad endometrial de un ratón durante la ventana de implantación.

Biomarcadores Salivales en Pacientes Diagnosticados con Fibrosis Quística, Concepción, 2016 / Salivary Biomarkers in Patients Diagnosed with Cystic Fibrosis, Concepción, 2016

RESUMEN: El odontólogo como profesional integral del área de la salud, debe tener conocimiento acerca de distintas manifestaciones bioquímicas que pueden tener repercusión en la cavidad oral. El objetivo del trabajo fue determinar las manifestaciones bioquímicas y alteraciones en biomarcadores salivales en la cavidad oral producto de la fibrosis quística o del consumo crónico de medicamentos para el tratamiento de la FQ. Se seleccionó un total de cinco personas con fibrosis quística y cuatro personas sanas, pertenecientes a la ciudad de Concepción en la Octava Región de Chile. Se midió pH salival, capacidad buffer, concentración de proteínas totales, tasa de flujo salival estimulado y se determinó presencia de ciertas enzimas salivales en pacientes que padecen la enfermedad. Se pudo evidenciar que el pH salival en sujetos con fibrosis quística tiende a ser mayor a los valores de referencia, la tasa de flujo salival es mucho menor al igual que la capacidad buffer, la concentración de proteínas totales en saliva se encuentra igual a los valores de referencia y se determinó la presencia biomarcadores salivales a través de la técnica de electroforesis. La fibrosis quística afecta de muchas formas a las personas que la padecen, genera cambios a nivel de los biomarcadores salivales como también en la cavidad oral, por lo que el odontólogo debe estar capacitado para identificar estos cambios y poder tratar de la mejor manera a todo tipo de paciente.

ABSTRACT: The dentist as an integral health professional must have knowledge of various biochemical manifestations that may have repercussions on the oral cavity. The objective of the study was to determine the biochemical manifestations and salivary biomarker alterations in the oral cavity resulting from cystic fibrosis or chronic consumption of drugs for the treatment of CF. We selected a total of five people with cystic fibrosis and four healthy people, from the city of Concepcion in the eighth region of Chile. Salivary pH, buffer capacity, total protein concentration, stimulated salivary flow rate and the presence of certain salivary enzymes were measured in patients suffering from the disease. It was observed that the salivary pH in subjects with cystic fibrosis tends to be higher than the reference values, the salivary flow rate and buffer capacity are less than normal, the total protein concentration in saliva is equal to the reference values and the presence of salivary biomarkers was determined through the electrophoresis technique. Cystic fibrosis affects those who suffer the disease in many ways, it generates changes at the salivary biomarker level, as well as in the oral cavity. The dentist must therefore, be able to identify these changes in order to treat them in the best possible approach for all types of patients.

Production of recombinant human epidermal growth factor in Pichia pastoris

Abstract This study was carried out to express human epidermal growth factor (hEGF) in Pichia pastoris GS115. For this aim, the hEGF gene was cloned into the pPIC9K expression vector, and then integrated into P. pastoris by electroporation. ELISA-based assay showed that the amount of hEGF secreted into the medium can be affected by the fermentation conditions especially by culture medium, pH and temperature. The best medium for the optimal hEGF production was BMMY buffered at a pH range of 6.0 and 7.0. The highest amount of hEGF with an average yield of 2.27 µg/mL was obtained through an induction of the culture with 0.5% (v/v) methanol for 60 h. The artificial neural network (ANN) analysis revealed that changes in both pH and temperature significantly affected the hEGF production with the pH change had slightly higher impact on hEGF production than variations in the temperature.

Difference in EGFR expression and mean vascular density in normal oral mucosa, oral epithelial dysplasia and oral squamous cell carcinoma

To evaluate the expression of the epidermal growth factor receptor (EGFR) and mean vascular density (MVD) in normal oral mucosa (NOM), oral epithelial dysplasia (OED) and oral squamous cell carcinoma (OSCC). Material and methods: Descriptive case study. Nineteen histological samples diagnosed with NOM, 18 diagnosed with OED, and 19 with OSCC, were analyzed with immunohistochemistry against EGFR and CD31. EGFR expression was evaluated by extent and intensity of its expression in normal, dysplastic and neoplastic epithelium. MVD was determined through the detection of blood vessels by antibodies against CD31. Results: Extension of EGFR expression was highest in OSCC followed by OED and lowest in NOM, resulting in significant different between the degrees of extension (p<0.001). Intensity of EGFR was similar in NOM, OED and OSCC, without differences in its expression (p=0.533). Differences in MVD were found between NOM and OSCC groups (p<0.01), and between OED and OSCC groups (p<0.01), with no differences between NOM and OED groups (p=0.91). MVD was 21.17 +/- 4.98 in NOM, 23.40 +/- 5.77 in OED and 33.92 +/- 8.39 in OSCC. Conclusion: EGFR is expressed in normal, dysplastic or neoplastic oral epithelium. However, the extent of its expression is greater as malignancy increases. MVD varies according to the diagnosis.

EGF Induced RET Inhibitor Resistance in CCDC6-RET Lung Cancer Cells

PURPOSE: Rearrangement of the proto-oncogene rearranged during transfection (RET) has been newly identified potential driver mutation in lung adenocarcinoma. Clinically available tyrosine kinase inhibitors (TKIs) target RET kinase activity, which suggests that patients with RET fusion genes may be treatable with a kinase inhibitor. Nevertheless, the mechanisms of resistance to these agents remain largely unknown. Thus, the present study aimed to determine whether epidermal growth factor (EGF) and hepatocyte growth factor (HGF) trigger RET inhibitor resistance in LC-2/ad cells with CCDC6-RET fusion genes. MATERIALS AND METHODS: The effects of EGF and HGF on the susceptibility of a CCDC6-RET lung cancer cell line to RET inhibitors (sunitinib, E7080, vandetanib, and sorafenib) were examined. RESULTS: CCDC6-RET lung cancer cells were highly sensitive to RET inhibitors. EGF activated epidermal growth factor receptor (EGFR) and triggered resistance to sunitinib, E7080, vandetanib, and sorafenib by transducing bypass survival signaling through ERK and AKT. Reversible EGFR-TKI (gefitinib) resensitized cancer cells to RET inhibitors, even in the presence of EGF. Endothelial cells, which are known to produce EGF, decreased the sensitivity of CCDC6-RET lung cancer cells to RET inhibitors, an effect that was inhibited by EGFR small interfering RNA (siRNA), anti-EGFR antibody (cetuximab), and EGFR-TKI (Iressa). HGF had relatively little effect on the sensitivity to RET inhibitors. CONCLUSION: EGF could trigger resistance to RET inhibition in CCDC6-RET lung cancer cells, and endothelial cells may confer resistance to RET inhibitors by EGF. E7080 and other RET inhibitors may provide therapeutic benefits in the treatment of RET-positive lung cancer patients.

Hepato-protective effect of rutin via IL-6/STAT3 pathway in CCl4-induced hepatotoxicity in rats

BACKGROUND: Carbon tetrachloride (CCl4) induces hepatotoxicity in animal models, including the increased blood flow and cytokine accumulation that are characteristic of tissue inflammation. The present study investigates the hepato-protective effect of rutin on CCl4-induced hepatotoxicity in rats. RESULTS: Forty male Wistar rats were divided into four groups. Group I (control group) received 1 mL/kg of dimethyl sulfoxide intragastrically and 3 mL/kg olive oil intraperitoneally twice a week for 4 weeks. Group II received 70 mg/ kg rutin intragastrically. Groups III and IV received CCl4 (3 mL/kg, 30 % in olive oil) intraperitoneally twice a week for 4 weeks. Group IV received 70 mg/kg rutin intragastrically after 48 h of CCl4 treatment. Liver enzyme levels were determined in all studied groups. Expression of the following genes were monitored with real-time PCR: interleukin-6 (IL-6), dual-specificity protein kinase 5 (MEK5), Fas-associated death domain protein (FADD), epidermal growth factor (EGF), signal transducer and activator of transcription 3 (STAT3), Janus kinase (JAK), B-cell lymphoma 2 (Bcl2) and B-cell lymphoma-extra-large (Bcl-XL). The CCl4 groups showed significant increases in biochemical markers of hepatotoxicity and up-regulation of expression levels of IL-6, Bcl-XL, MEK5, FADD, EGF, STAT3 and JAK compared with the control group. However, CCl4 administration resulted in significant down-regulation of Bcl2 expression compared with the control group. Interestingly, rutin supplementation completely reversed the biochemical markers of hepatotoxicity and the gene expression alterations induced by CCl4. CONCLUSION: CCl4 administration causes alteration in expression of IL-6/STAT3 pathway genes, resulting in hepatotoxicity. Rutin protects against CCl4-induced hepatotoxicity by reversing these expression changes.

Phospholipase D activates HIF-1-VEGF pathway via phosphatidic acid

Growth factor-stimulated phospholipase D (PLD) catalyzes the hydrolysis of phosphatidylcholine (PC), generating phosphatidic acid (PA) which may act as a second messenger during cell proliferation and survival. Therefore, PLD is believed to play an important role in tumorigenesis. In this study, a potential mechanism for PLD-mediated tumorigenesis was explored. Ectopic expression of PLD1 or PLD2 in human glioma U87 cells increased the expression of hypoxia-inducible factor-1alpha (HIF-1alpha) protein. PLD-induced HIF-1 activation led to the secretion of vascular endothelial growth factor (VEGF), a HIF-1 target gene involved in tumorigenesis. PLD induction of HIF-1alpha was significantly attenuated by 1-butanol which blocks PA production by PLD, and PA per se was able to elevate HIF-1alpha protein level. Inhibition of mTOR, a PA-responsive kinase, reduced the levels of HIF-1alpha and VEGF in PLD-overexpressed cells. Epidermal growth factor activated PLD and increased the levels of HIF-1alpha and VEGF in U87 cells. A specific PLD inhibitor abolished expression of HIF-1alpha and secretion of VEGF. PLD may utilize HIF-1-VEGF pathway for PLD-mediated tumor cell proliferation and survival.

Immunolocalization of HB-EGF in human skin by streptavidin-peroxidase (HRP) conjugate method / Inmunolocalización de HB-EGF en piel humana por el método de conjugado estreptavidina-peroxidasa (HRP)

EGF family growth factors consists of growth factors, such as transforming growth factor (TGF)-a, heparin-binding EGF-like growth factor (HB-EGF), amphiregulin (AR) and epiregulin, autocrine growth factors in normal human keratinocytes. HB-EGF is mitogen for epithelial cells and like other members of the EGF family, HB-EGF exerts its biological effects via interaction with the EGF receptor (EGFR). HB-EGF is an autocrine growth factor for human keratinocytes, and has a possible role as a paracrine growth factor for fibroblast. Our report concerning immunohistochemical localization of HB-EGF in normal skin by using the streptavidin-peroxidase (HRP) conjugate method, confirms previous data, revealing specific patterns of HB-EGF localization. Identification of HB-EGF in cells of epithelial origin suggests its autocrine and/or paracrine roles in epithelial cell maintenance. Our report especially wants to give a technical contribution, easy to manage and with evident results. A simple technique that does not require use of sophisticated equipment.

La familia factores de crecimiento EGF se compone de representantes como el factor de crecimiento transformante (TGF)-a, factor epidérmico vinculante a la heparina (HB-EGF), anfiregulina (AR) y epirregulina, factores autocrinos de crecimiento en queratinocitos humanos normales. HB-EGF es mitógeno para células epiteliales y al igual que otros miembros de la familia EGF, HB-EGF ejerce sus efectos biológicos a través de la interacción con el receptor de EGF (EGFR). HB-EGF es un factor de crecimiento autocrino de queratinocitos humanos, y tiene un posible papel como factor de crecimiento paracrino de los fibroblastos. Nuestro reporte sobre la localización inmunohistoquímica de HB-EGF en la piel normal mediante el método de conjugado estreptavidina-peroxidasa (HRP), confirma datos anteriores, revelando patrones de localización específicos para HB-EGF. La identificación de HB-EGF en las células de origen epitelial sugiere su papel autocrino y/o paracrinos en el mantenimiento de las células epiteliales. Nuestro informe quiere dar una contribución técnica, fácil de manejar y con resultados evidentes. Una técnica simple que no requiera el uso de equipo sofisticado.

Novel neurotrophic factor secreted by amniotic epithelial cells

By virtue of expressions of glial and neural surface markers and capability of neurotransmitter metabolism, amniotic epithelial cells are considered as candidate cell type for transplantation strategies to treat neurological disorders. Previously, we have reported neurotrophism exhibited by human amniotic epithelial cells when transplanted after spinal cord injury in bonnet monkeys. Amniotic epithelial cells were believed to secrete an "Epidermal Growth Factor (EGF)-like" factor and exact identification was not made. At this juncture, through the present study it was found that, chicken neural retinal cells when grown alone failed to survive and contrarily when either co-cultured with chicken amniotic epithelial cells/cultured in amniotic epithelial cell conditioned medium not only survived but also showed extensive differentiation. Fibroblast Growth Factor-2 (FGF-2) plays a critical role in retinal development especially in chicken neural retinal development. However, immunoassay using western blot did not revealed the presence of any already known isoforms of FGF-2 in the medium. It is interesting to note that while factor secreted by amniotic epithelial cells resembles EGF and/or FGF-2 in its biological action, known isoforms of them were not detected. Considering the biological closeness between EGF and FGF-2, results indicate the possibility of a novel isoform of these growth factors secreted by amniotic epithelial cells. Further studies will establish the nature of this novel factor which will enhance the application of this interesting cell type for neural transplantations.

Epidermal growth factor receptors, testosterone levels and parotid gland changes in rats infected with Trypanosoma cruzi

It has been demonstrated that parotid glands of rats infected with Trypanosoma cruzi present severe histological alterations; changes include reduction in density and volume of the acini and duct systems and an increase in connective tissue. We evaluated the association between morphological changes in parotid glands, circulating testosterone levels and epidermal growth factor receptor (EGF-R) expression in experimental Chagas disease in rats. Animals at 18 days of infection (acute phase) showed a significant decrease in body weight, serum testosterone levels and EGF-R expression in the parotid gland compared with a control group. Since decreases in body weight could lead to a reduction in circulating testosterone concentration, we believe that the reduction in EGF-R expression in parotid glands of infected rats is due to alterations in testosterone levels and atrophy of parotid glands is caused by changes in EGF-R expression. Additionally, at 50 days (chronic phase) of infection parotid glands showed a normal histological aspect likely due to the normalization of the body weight. These findings suggest that the testosterone-EGF-R axis is involved in the histological changes.

Role of STAT3 as a Negative Regulator in Mac2- Binding Protein Expression / 대한진단검사의학회지

BACKGROUND: Mac-2 binding protein (Mac-2BP) is a secreted glycoprotein from the culture fluid of several human cancer cells, especially breast, lung, and gastric cells. Mac-2BP plays a role in immune response and cell adhesion activity in patients with various cancer and infectious diseases. In this study, we attempted to identify the regulators of Mac-2BP expression at the transcriptional level. METHODS: To determine the effect of epidermal growth factor (EGF) to Mac-2BP expression in gastric cancers, we constructed the different lengths of Mac-2BP promoter plasmids and measured the promoter activity and Mac-2BP expression. In addition to investigating the role of signal transducer and activator of transcription3 (STAT3) or human telomerase reverse transcriptase (hTERT) as a regulator of Mac-2BP, we transfected the small interfering RNA (siRNA) specific for STAT3 or hTERT, and Mac-2BP level was observed by a quantitative ELISA. RESULTS: EGF treatment could suppress the Mac-2BP transcription in HEK293 or gastric cancer cell lines (SNU-638 or AGS). In 5'-deleted promoter experiment, pGL3-Mac Pro-2377 transfected cells showed a decreased luciferase activity compared to pGL3-Mac Pro-2277. We also identified that (-2,366/-2,356) on Mac-2BP promoter is a putative STAT3 binding site and suppression of STAT3 with STAT3 specific siRNA increased the Mac-2BP level, suggesting the role of STAT3 as a negative regulator, in contrast to hTERT, which is known as a positive regulator. CONCLUSIONS: EGF signal is critical for the Mac-2BP expression, and more importantly, STAT3 could work as a negative regulator, while hTERT as a positive regulator in Mac-2BP transcription.

Relevance of iodine intake as a reputed predisposing factor for thyroid cancer

Iodine is a trace element that is essential for the synthesis of thyroid hormone. Both chronic iodine deficiency and iodine excess have been associated with hypertrophy and hyperplasia of follicular cells, attributed to excessive secretion of TSH. This may be associated to thyroid cancer risk, particularly in women. Experimental studies have documented thyroid cancer induction by elevation of endogenous TSH, although in a small number of animals. Iodine deficiency associated with carcinogenic agents and chemical mutagens will result in a higher incidence of thyroid malignancy. Inadequate low iodine intake will result in increased TSH stimulation, increased thyroid cell responsiveness to TSH, increased thyroid cell EGF-induced proliferation, decreased TGFbeta 1 production and increased angiogenesis, all phenomena related to promotion of tumor growth. Epidemiological studies associating iodine intake and thyroid cancer led to controversial and conflicting results. There is no doubt that introduction of universal iodine prophylaxis in population previously in chronic iodine-deficiency leads to a changing pattern of more prevalent papillary thyroid cancer and declining of follicular thyroid cancer. Also anaplastic thyroid cancer is practically not seen after years of iodine supplementation. Iodine excess has also been indicated as a possible nutritional factor in the prevalence of differentiated thyroid cancer in Iceland, Hawaii and, more recently, in China. In conclusion: available evidence from animal experiments, epidemiological studies and iodine prophylaxis has demonstrated a shift towards a rise in papillary carcinoma, but no clear relationship between overall thyroid cancer incidence and iodine intake.

O iodo é essencial para a síntese de hormônios tireóideos e tanto a deficiência crônica deste halogeno como o excesso nutricional de iodo levam a hiperplasia e hipertrofia dos elementos foliculares (por excesso de TSH). Esse fenômeno pode se associar a maior risco de câncer de tireóide, especialmente no sexo feminino. Estudos experimentais documentam indução de câncer de tireóide após prolongado excesso circulante de TSH, o qual induz aumento da proliferação celular medida por fator de crescimento epidermal (EGF), decréscimo de síntese de fator de transformação do crescimento (TGFbeta 1) e aumento da angiogenese. Estudos epidemiológicos entre nutrição de iodo e câncer de tireóide são conflitantes. É, todavia, aceito que a correção de prévia deficiência de iodo com aporte nutricional adequado deste halogeno leva à maior prevalência de carcinoma papilífero (e decréscimo de carcinoma folicular). Em alguns países, o excesso de iodo foi apontado como causa aparente de maior prevalência de câncer de tireóide. Em conclusão: não existe uma relação causa-efeito entre iodo nutricional e prevalência de câncer de tireóide, e outros fatores intervenientes ambientais devem ser considerados.

Mucin secretion in the rat tracheal epithelial cells by epidermal growth factor and Pseudomonas aeruginosa extracts

BACKGROUND: Hypersecretion of mucin due to goblet cell hyperplasia is frequently encountered in many chronic airway diseases, such as chronic bronchitis, bronchiectasis, bronchial asthma and cystic fibrosis. Even in normal individuals, viral infection or bacterial pneumonia frequently provoke huge amounts of bronchial secretions which may cause airway obstruction. The production of mucin was regulated by epidermal growth factor (EGF) in vitro. To know whether this EGF system regulates mucin secretion in vivo and Pseudomonas also stimulates the mucin secretion by the same pathway, we studied these relationships in the cultured rat tracheal epithelial cells. METHODS: Rat tracheal epithelial cells were obtained by pronase dissociation from the male Fisher 344 rats. When cells became confluent, they were divided into 6 groups and stimulated with either EGF for 24 hours or Pseudomonas extracts for 12 hours with or without selective EGF-R tyrosine kinase inhibitor tyrphostin AG1478. RESULTS: We found that both EGF and Pseudomonas extracts phosphorylated the tyrosine residue in the EGF receptor from the rat tracheal epithelial cells and this tyrosine phosphorylation was nearly completely blocked by selective EGF-R tyrosine kinase inhibitor tyrphostin AG1478. The mucin secretion was also stimulated by either EGF or Pseudomonas extracts but more strong secretion of mucin and MUC5AC gene expression in the rat tracheal epithelial cell was done by Pseudomonas extracts. CONCLUSION: These data suggest that Pseudomonas secretes the mucin by way of the EGF receptor and MUC5AC gene expression and the inhibitors of EGF receptor tyrosine phosphorylation would be useful to prevent the huge production of mucin due to Pseudomonas aeruginosa lung infection.

Importância do fator de crescimento epidérmico (EGF) e seu receptor (EGF-R) no tecido endometrial / Epidermal growth factor (EGF) and its receptor (EGF-R) importance in the endometrial tissue

Os autores fazem uma revisäo sobre a influência que o EGF e seu receptor (EGF-R) exercem no tecido endometrial, enfocando sua possível regulaçäo pelos esteróides e seus receptores e sua importância nos processos de transformaçäo secretora e de decidualizaçäo.

Epidermal growth factor and gastrin in scleroderma/CREST syndrome

Background. The objective of this study was to determine levels of epidermal growth factor (EGF) and gastrin (GA) in saliva, serum, and urine in scleroderma (Scl) and CREST syndrome. Methods. EGF and GA levels were mesured by radioimmunoassay in saliva, serum and urine in 10 patients (51 years, median; range, 35-66 years); 9 females and 1 male with Scl, 3 females with CREST syndrome, and 18 age-and sex-matched controls, 17 females and 1 male free of any systemic inflammatory disease. Results. In serum, the EGF was lower in Scl/CREST than controls (p=0.02), while GA serum concentrations were higher in Scl/CREST (p=0.02). In urine, EGF in Scl/CREST was slightly lower than controls (p=NS) and GA concentrations were higher than controls (p=0.03). In saliva, the EGF levels in Scl/CREST were also slightly lower than controls (p=NS), while GA concentrations in both Scl/CREST and controls were not different (p=NS). Conclusions. Low concentrations of EGF in serum probably play a role in the pathogenesis of Scl/CREST. GA concentration can be increased as a consequence of the low levels of EGF because of the structural homology of this peptide with urogastrone, a GA inhibitor factor

Acción del factor de crecimiento epidérmico sobre el desarrollo de las células estriatales cultivadas / Epidermal growth factor effects on striatal cells cultures

En este trabajo se describe la acción del factor de crecimiento epidérmico (FCE) sobre las células del estriado embrionario en un sistema de cultivo disociado de neuronas y glías. El cultivo de células se preparó a partir de embriones de ratas de 16-17 días. En el sistema de cultivo empleado, la población celular fue cultivada durante 20-24 horas en un medio que contenía suero y, y posteriormente, fue tratada con 20 ng/mL del FCE en un medio libre de suero. La eliminación del suero en este período inicial de desarrollo provocó una disminución apreciable de las células vivas en los cultivos tratados y en los controles. Al parecer, la población de células sobrevivientes estaba integrada, en su mayoría, por precursores celulares teniendo en cuenta su capacidad proliferativa. La acción del FCE sobre las células se manifestó en un aumento del número de células debido fundamentalmente a un estímulo de la proliferación de los precursores neuronales y astrocitos. Este efecto estuvo acompañado por una reducción de la diferenciación morfológica neural cuando se comparó con los cultivos controles. En los cultivos, a los 16 días, la detección de la actividad específica de la colina acetiltrasferasa evidenció la diferenciación de una subpoblación neural colinérgica, las cuales respondieron al tratamiento con el factor de crecimiento nervioso con un aumento de la actividad de la enzima