Time filter

Source Type

Zhang W.Y.,Changning Maternity and Infant Health Hospital
Zhonghua fu chan ke za zhi | Year: 2010

To study the clearance of high risk human papillomavirus (HPV) infection among the women with normal cervical pathologic diagnosis. One hundred and seventy-two HPV-positive cases with normal cervical pathologic diagnosis were enrolled in the study. The infection status of HPV was monitored during follow-up from Aug 2006 to Aug 2008. The time of HPV infection spontaneous clearance, as well as effect factors, were analyzed. During follow-up, there were 62.2% (107 cases, 107/172) of the HPV infection cleared. The medium clearance time was 11.3 months (95%CI: 10.6 - 16.6 months). The medium clearance time of aged < 30 years, 30 - 39 years, 40 - 49 years and > 49 years were 11.3, 12.0, 10.9 and 8.5 months, respectively. There were not significant difference among aged intervals (P = 0.384). The virus copies of HPV-clearance cases and persistent-infection were 22.6 and 95.0, respectively. There was not significant difference between groups (P = 0.061). Most of the high risk HPV infection with normal cervical pathologic diagnosis would spontaneously cleared. Age and HPV copies may play little role in the HPV clearance.

Xue Y.,Papillomavirus Regulation and Cancer | Bellanger S.,Papillomavirus Regulation and Cancer | Zhang W.,Changning Maternity and Infant Health Hospital | Lim D.,National University Hospital Singapore | And 3 more authors.
Cancer Research | Year: 2010

The viral E2 gene product plays a crucial role in the human papillomavirus (HPV) vegetative cycle by regulating both transcription and replication of the viral genome. E2 is a transcriptional repressor of the E6 and E7 viral oncogenes for HPV types 16 and 18, which are involved in cervical cancers. Using new polyclonal antibodies against the HPV16 E2 protein, we showed that E2 is expressed at various precursor stages of cervical carcinoma by immunohistochemistry on paraffin-embedded clinical samples. E2 was found to be highly expressed in the nuclei and cytoplasm of cells forming the intermediate and upper layers of cervical intraepithelial neoplasia (CIN). We could show that the expressions of E2 and p16INK4a (surrogate marker for oncogenic E7 expression) were exclusive in most of the cases, thus implying that E2 is not expressed together with high levels of E7. Moreover, we found that E2 is expressed in a subset of columnar cells adjacent to the CIN. We could show that expression of E2 is topologically distinct from the proliferation markers p63 and Ki67, whereas it coincides with the expression of cytokeratin K13, a marker of squamous cell differentiation. Expression of E2 also topologically coincides with episomal amplification of viral genomes in the upper layers of CIN1. These in vivo data thus validate previous assumptions of the crucial role of E2 in the early steps of HPV infection and of its negative link with expression of the viral E6 and E7 oncogenes. ©2010 AACR.

Shu Q.,Changning Maternity and Infant Health Hospital | Li W.,Changning Maternity and Infant Health Hospital | Li J.,Fudan University | Wang W.,Fudan University | And 2 more authors.
PLoS ONE | Year: 2014

Overexposure of the fetus to glucocorticoids in gestation is detrimental to fetal development. The passage of maternal glucocorticoids into the fetal circulation is governed by 11beta-Hydroxysteroid Dehydrogenase Type 2 (HSD11B2) in the placental syncytiotrophoblasts. Human chorionic gonadotropin (hCG) plays an important role in maintaining placental HSD11B2 expression via activation of the cAMP pathway. In this study, we investigated the relationship between the activation of the cAMP pathway by hCG and subsequent phosphorylation of extracellular signal-regulated kinase1/2 (ERK1/ 2) or p38 mitogen-activated protein kinase (MAPK) pathways in the regulation of placental HSD11B2 expression in human placental syncytiotrophoblasts. We found that treatment of the placental syncytiotrophoblasts with either hCG or dibutyl cAMP (dbcAMP) could promote the phosphorylation of p38 and ERK1/2. Inhibition of p38 MAPK with SB203580 not only reduced the basal HSD11B2 mRNA and protein levels but also attenuated HSD11B2 levels induced by either hCG or dbcAMP. By contrast, inhibition of ERK1/2 with PD98059 increased the basal mRNA and protein levels of HSD11B2 and had no effect on HSD11B2 mRNA and protein levels induced by either hCG or dbcAMP. These data suggest that p38 MAPK is involved in both basal and hCG/cAMP-induced expression of HSD11B2, and ERK1/2 may play a role opposite to p38 MAPK at least in the basal expression of HSD11B2 in human placental syncytiotrophoblasts and that there is complicated cross-talk between hCG/cAMP and MAPK cascades in the regulation of placental HSD11B2 expression. © 2014 Shu et al.

Liu P.,Changning Maternity and Infant Health Hospital | Qi M.,Chinese Academy of Sciences | Ma C.,Changning Maternity and Infant Health Hospital | Lao G.,Changning Maternity and Infant Health Hospital | Liu Y.,Changning Maternity and Infant Health Hospital
FEBS Letters | Year: 2013

MicroRNAs negatively regulate target gene expression at the post-transcriptional level during carcinogenesis. Recent advances revealed that the expression levels of several miRNAs are up- or down-regulated in endometrial carcinoma (EC). Here we identify dysregulated miRNAs in EC and we elucidate the essential role of let-7a. The expression of 86 miRNAs in EC was found to be different from adjacent normal endometrial tissues. Moreover, miR-let-7 members are down-regulated in EC and let-7 miRNAs are highly associated with endometrial cancer. A functional investigation revealed that let-7a suppressed proliferation of HeLa cells by targeting Aurora-B. Let-7a also antagonizes Aurora-B functions in promoting carcinoma cell proliferation by down-regulating Aurora-B protein level. Let-7a could be applied for gene therapy against endometrial carcinogenesis. © 2013 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

Liu C.,Fudan University | Zhu P.,No.401 Hospital | Wang W.,Shanghai JiaoTong University | Li W.,Changning Maternity and Infant Health Hospital | And 5 more authors.
Molecular and Cellular Endocrinology | Year: 2016

The underlying mechanism leading to rupture of the membranes at parturition is not fully understood. Lysyl oxidase (LOX) cross-links collagen fibrils thereby increasing the tensile strength of the membranes. Thus, understanding the regulation of LOX expression may be of crucial importance for elucidation of the process of rupture of the fetal membranes. Prostaglandin E2 (PGE2), mainly produced in the amnion, plays crucial roles during human parturition. However it is not known whether PGE2 regulates LOX expression in the fetal membranes. Using primary human amnion fibroblasts, we showed that addition of PGE2 decreased LOX mRNA and protein levels, which were blocked by inhibition of EP2/EP4 receptors and the receptor-coupled cAMP/PKA pathway. EP2/EP4 receptor agonists and stimulators of the cAMP/PKA pathway consistently decreased LOX expression. Furthermore, PGE2 induced cyclo-oxygenase-2 (COX-2) expression, a key enzyme in PGE2 production, via an EP2 and EP4 receptor-coupled cAMP/PKA pathway. Small interfering RNA-mediated knock-down of COX-2 expression significantly increased the basal expression of LOX. In addition, an increase in COX-2 and a reciprocal decrease in LOX abundance occurred in amnion tissue following labor at term. In conclusion, we have revealed a feed-forward loop of induction of COX-2 and reduction in LOX expression by PGE2 acting via an EP2/EP4 receptor-coupled cAMP/PKA pathway in human amnion fibroblasts toward the end of gestation, which may play a significant role in the rupture of fetal membranes. © 2016 Elsevier Ireland Ltd.

Discover hidden collaborations