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1.
Korean Journal of Obstetrics and Gynecology ; : 237-244, 2009.
Article in Korean | WPRIM | ID: wpr-120708

ABSTRACT

OBJECTIVE: This study was performed to investigate the expression of EGF mRNA and protein in eutopic and ectopic endometrial tissues of the patients with endometriosis and in eutopic endometrial tissues of the patients without endometriosis. METHODS: Study group was composed of 34 women with endometriosis taking surgical treatment at the Department of Obstetrics and Gynecology, Asan Medical Center, from October 2004 to December 2005. Control group consisted of 14 women who had undergone surgical treatment for cervical intraepithelial neoplasia or benign gynecologic conditions other than endometriosis during the same period. Eutopic endometrial tissues of both groups and ectopic endometrial tissues of study group were collected during the operations. Real time reverse transcriptase-polymerase chain reaction (RT-PCR) was used to quantify EGF mRNA of these tissues. Western blot analysis was performed to ascertain the expression of EGF protein. RESULTS: The expressions of EGF mRNA were significantly lower in both eutopic (P<0.01) and ectopic (P<0.01) endometrial tissues of the women with endometriosis than in eutopic endometrial tissues of control group. The expressions of EGF protein were shown to be lower in both eutopic and ectopic endometrial tissues of the women with endometriosis than in eutopic endometrial tissues of control group. CONCLUSION: We found some correlations between the lower expression of EGF in endometrial tissues and the development of endometriosis. In addition, the change or defect of some factors in the eutopic endometrium might play an important role in the development of endometriosis.


Subject(s)
Female , Humans , Blotting, Western , Uterine Cervical Dysplasia , Endometriosis , Endometrium , Epidermal Growth Factor , Gynecology , Obstetrics , RNA, Messenger
2.
The Korean Journal of Internal Medicine ; : 167-172, 2001.
Article in English | WPRIM | ID: wpr-153771

ABSTRACT

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.


Subject(s)
Male , Rats , Animals , Blotting, Western , Cells, Cultured , Comparative Study , Epidermal Growth Factor/metabolism , Epithelial Cells/drug effects , Gene Expression , Models, Animal , Mucins/drug effects , Pseudomonas aeruginosa , RNA, Messenger/analysis , Rats, Inbred F344 , Reverse Transcriptase Polymerase Chain Reaction , Sensitivity and Specificity , Trachea/cytology
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