title: [Extracellular signal-regulated protein kinase activation in endometrium with polycystic ovary syndrome and its significance].
abstract: OBJECTIVE
  to investigate the activation of mitogen-activated protein kinase (MAPK)/extracellular signal-regulated protein kinase (ERK) signaling pathway in the endometrium of women with polycystic ovary syndrome (PCOS) and its effect and significance in the cause of hyperplasia and carcinoma; and investigate the factors which affect the activation of the MAPK/ERK signaling pathway.
  
  
  METHODS
  collected 52 patients diagnosed as PCOS who were taken dilation and curettage of uterus as study, while 32 non-PCOS patients matched as control group. Serum hormonal parameters, fasting blood glucose and insulin were measured in all patients. The PCOS patients were sub-group as insulin resistance group and non-insulin resistance group; all the patients were carried out pathology inspection of endometria, and the PCOS patients were sub-group as endometrial hyperplasia and carcinoma group and normal endometrium group based on the outcome of pathology inspection. Western blot were performed to detect the expressions of ERK1/2 and phosphorylated ERK1/2 (p-ERK1/2), the activation of ERK1/2.
  
  
  RESULTS
  (1) the expression of p-ERK1/2 [(61 ± 13)%] in the endometrium in PCOS group was higher than that in the control [(44 ± 10)%, P < 0.01]. (2) The expression of p-ERK1/2 was significantly increased in group of endometrial hyperplasia and carcinoma [(70 ± 11)%] compared to that in group of normal endometrium [(55 ± 10)%, P < 0.01], while there were significant difference between group of insulin resistance [(63 ± 13)%] and group of non-insulin resistance [(55 ± 7)%, P < 0.01]. (3)Fasting insulin level, insulin area under the curve and body mass index were related to the expression of p-ERK1/2 in endometrium with PCOS, the correlation coefficient were 0.447, 0.456 and 0.381, respectively (all P < 0.01).
  
  
  CONCLUSIONS
  the MAPK/ERK signaling pathway in endometrium with PCOS was overactivation, which was related to the endometrial hyperplasia and carcinoma; while the activation of MAPK/ERK signaling pathway were effected by insulin resistance and hyperinsulinemia.
authors.affiliation: Department of Obstetrics and Gynecology, General Hospital, Tianjin Medical University, Tianjin 300052, China. songxr63@yahoo.com.cn
authors.forename: Xue-Ru
authors.initials: XR
authors.lastname: Song
authors.forename: Hui-Ying
authors.initials: HY
authors.lastname: Zhang
authors.forename: Yan-Fang
authors.initials: YF
authors.lastname: Zhang
authors.forename: Yu-Kun
authors.initials: YK
authors.lastname: Han
authors.forename: Ke-Jun
authors.initials: KJ
authors.lastname: Li
mesh_terms: D001786:Blood Glucose / Q000378:metabolism; D015153:Blotting, Western; D004714:Endometrial Hyperplasia / Q000378:metabolism*; D016889:Endometrial Neoplasms / Q000378:metabolism; D004717:Endometrium / Q000378:metabolism*; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism*; D005260:Female; D006801:Humans; D006946:Hyperinsulinism / Q000378:metabolism; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism; D010766:Phosphorylation; D011085:Polycystic Ovary Syndrome / Q000378:metabolism*; D015398:Signal Transduction
chemical_list: D001786:Blood Glucose; D007328:Insulin; D048049:Extracellular Signal-Regulated MAP Kinases; D020928:Mitogen-Activated Protein Kinases