Zhang T.,Shaoxing Women and Childrens Hospital |
Fang M.,Shaoxing Women and Childrens Hospital |
Fu Z.-M.,Shaoxing Women and Childrens Hospital |
Du H.-C.,Shaoxing Women and Childrens Hospital |
And 4 more authors.
Asian Pacific Journal of Tropical Medicine | Year: 2014
Objective: To analyze the expression of phosphatidylinositol 3 kinase (PI3-K), protein kinase B (PKB) and glycogen synthase kinase 3 beta (GSK-3 β) in skeletal muscle tissue of gestational diabetes mellitus (GDM). Methods: A total of 90 cases of pregnant women were divided into observation group and control group according to the occurrence of GDM with 45 cases in either, and the expression of PI3-K, PKB, GSK-3 β mRNA expression in skeletal muscle tissue was compared between two groups. Results: The total PI3-K p85 protein was significantly higher in the observation group compared with the control group, the activity of PI3-K was lower than that of the latter; The total PKB, GSK-3 β protein in skeletal tissue had no significant difference between two groups, while the serine phosphorylation levels of PKB and GSK-3βwere significantly lower in observation group compared with the control group. Conclusions: The downregulation of PI3-K, PKB and GSK-3βin skeletal tissue of GDM caused by phosphorylation dysfunction of signaling molecules is the reason for insulin resistance and transporter function decline which lead to GDM. © 2014 Hainan Medical College.
PubMed | Shanghai JiaoTong University, Ningbo Women and Childrens Hospital, Huzhou Maternity and Child Care Hospital, Jiaxing Maternity and Child Care Hospital and 3 more.
Type: | Journal: BMC medical genetics | Year: 2015
Offspring of pregnancy complicated with gestational diabetes (GDM) are at high risk for metabolic diseases. The mechanisms behind the association of intrauterine exposure to GDM and high risk of health problems in later life remain largely unknown. The aim of this study was to clarify the alteration in methylation levels at differentially methylated regions (DMRs) of GNAS and IGF2 in fetuses of GDM women and to explore the possible mechanisms linking maternal GDM with high risk of metabolic diseases in later life of GDM offspring.Lymphocytes were isolated from umbilical cord blood of infants born to 87 women with GDM and 81 women with normal pregnancy. Genomic DNA was extracted and DNA methylation levels of GNAS and IGF2 DMRs were determined by Massarray quantitative methylation analysis.The methylation levels were detected in 7 CpG sites of GNAS DMRs and 6 sites of IGF2 DMRs. Methylation levels were significantly higher at sites 4, 5 and 7 of GNAS DMR in GDM compared to normal pregnancy (P = 0.007, 0.008 and 0.008, respectively). The methylation level at site 4 of GNAS was significantly correlated with the presence of GDM (P = 0.003), the methylation levels at site 5 and 7 were significantly correlated with the presence of GDM (P = 0.002 for both) and gestational age (P = 0.027 for both). There was no significant difference in any sites of IGF2 DMR (P > 0.05 for all).We concluded maternal GDM-induced hypermethylation at GNAS DMR and this condition may be among the mechanisms associating maternal GDM with increased risk of metabolic diseases in later life of offspring.
PubMed | Linyi Peoples Hospital and Shaoxing Women and Childrens Hospital
Type: Journal Article | Journal: Asian Pacific journal of tropical medicine | Year: 2014
To analyze the expression of phosphatidylinositol 3 kinase (PI3-K), protein kinase B (PKB) and glycogen synthase kinase 3 beta (GSK-3 ) in skeletal muscle tissue of gestational diabetes mellitus (GDM).A total of 90 cases of pregnant women were divided into observation group and control group according to the occurrence of GDM with 45 cases in either, and the expression of PI3-K, PKB, GSK-3 mRNA expression in skeletal muscle tissue was compared between two groups.The total PI3-K p85 protein was significantly higher in the observation group compared with the control group, the activity of PI3-K was lower than that of the latter; The total PKB, GSK-3 protein in skeletal tissue had no significant difference between two groups, while the serine phosphorylation levels of PKB and GSK-3 were significantly lower in observation group compared with the control group.The downregulation of PI3-K, PKB and GSK-3in skeletal tissue of GDM caused by phosphorylation dysfunction of signaling molecules is the reason for insulin resistance and transporter function decline which lead to GDM.
PubMed | Linyi Peoples Hospital, Women and Childrens Health Care Hospital of Linyi and Shaoxing Women and Childrens Hospital
Type: Journal Article | Journal: Gene | Year: 2016
Osteosarcoma is the most common primary bone cancer which is associated with early metastatic potential and poor prognosis. However, the molecular mechanisms underlying osteosarcoma progression are not well characterized. Here, we investigated the role of miR-409-3p in osteosarcoma metastasis. Osteosarcoma tissue showed decreased expression of miR-409-3p compared to adjacent non-tumorous tissue. The expression level of miR-409-3p was negatively correlated with osteosarcoma metastasis. Overexpression of miR-409-3p in osteosarcoma cells (U2OS) inhibited cell migration and invasion. Bioinformatics analysis showed that catenin-1 (CTNND1, p120-catenin) is a direct target of miR-409-3p. Overexpression of miR-409-3p repressed the expression of catenin-1 in U2OS cells at both mRNA and protein levels. Meanwhile, miR-409-3p repressed the activity of luciferase reporter containing the 3-untranslated region (3UTR) of CTNND1 gene. Furthermore, expression of catenin-1 rescued the inhibitory effect of miR-409-3p on cell migration and invasion. Altogether, these results indicated that miR-409-3p targets catenin-1 to repress osteosarcoma metastasis.
PubMed | Shaoxing Women and Childrens Hospital, University of Southern California, Beckman Research Institute and Zhejiang University
Type: Journal Article | Journal: FASEB journal : official publication of the Federation of American Societies for Experimental Biology | Year: 2016
Flap endonuclease 1 (FEN1) phosphorylation is proposed to regulate the action of FEN1 in DNA repair as well as Okazaki fragment maturation. However, the biologic significance of FEN1 phosphorylation in response to DNA damage remains unknown. Here, we report an in vivo role for FEN1 phosphorylation, using a mouse line carrying S187A FEN1, which abolishes FEN1 phosphorylation. Although S187A mouse embryonic fibroblast cells showed normal proliferation under low oxygen levels (2%), the mutant cells accumulated oxidative DNA damage, activated DNA damage checkpoints, and showed G
Zeng Q.,Chinese PLA General Hospital |
Yuan Y.,Chinese Institute of Aviation Medicine |
Wang S.,Chinese PLA General Hospital |
Sun J.,Chinese PLA General Hospital |
And 2 more authors.
Canadian Journal of Cardiology | Year: 2013
Background: Genome-wide association studies have identified 2 single-nucleotide polymorphisms (SNPs) on chromosome arm 9p21, rs10757278, and rs2383207 that confer susceptibility to myocardial infarction. However, these data are mostly from Italian, American Caucasian, South Korean, and Japanese cohorts. This study is the firstto investigate whether 6 SNPs (rs10757277, rs10757278, rs10757279, rs1333049, rs1333047, and rs10811656) are associated with acute coronary syndrome (ACS) in a Chinese Han population. Methods: We performed a case-control analysis in 359 patients with ACS diagnosed by coronary angiography and 398 non-ACS controls of Han background between April 2007 and January 2008 to determine whether these 6 SNPs were associated with ACS. Exon fragments were genotyped by polymerase chain reaction-restriction fragment length polymorphism. Results: After we adjusted for clinical parameters, we found the rs10757278 GG genotype to be associated with a significantly elevated risk of ACS (odds ratio [OR], 1.91; 95% confidence interval [CI], 1.35-2.68; P= 0.00035), the rs10811656 T allele to be associated with a higher risk of ACS (OR, 1.67; 95% CI, 1.26-2.23; P= 0.0016) than the CC genotype, and the rs1333047 TT genotype also to be associated with a higher risk of ACS (OR, 1.57; 95% CI, 1.15-2.06; P= 0.0052) than the CC and CT genotypes. After 14.2 ± 4.5 months of follow-up, the end-point data were obtained: death (cardiac and noncardiac), nonfatal myocardial infarction, and recurrent angina leading to repeated coronary angiography. We found that the rs10757278 GG genotype was significantly associated with recurrent angina compared with the AA and AG genotypes (P= 0.013). Conclusions: Polymorphisms on 9p21 were associated with ACS in a Chinese Han population. The rs10757278 GG genotype was further associated with adverse cardiac outcomes after ACS. © 2013 Canadian Cardiovascular Society.
Zhang T.,Shaoxing Women and Childrens Hospital |
Liang W.,Shaoxing Peoples Hospital |
Fang M.,Shaoxing Women and Childrens Hospital |
Yu J.,Zhejiang Academy of Medical science |
And 2 more authors.
Gene | Year: 2013
Background: Many studies have reported the associations of polymorphic CAG repeats in androgen receptor (AR) gene with PCOS risk, but with inconsistent results. So, the aim of present meta-analysis was to clarify such inconsistence, so as to provide more conclusive results. Methods: PubMed was searched for the eligible reports published until February 2012 without language limitation. The studies reporting the relationship between CAG repeat length and PCOS were selected for the meta-analysis according to the inclusion criteria. Two reviewers independently extracted the data and evaluated the study quality. Principal findings: As for the relationship between CAG repeat length and PCOS risk, the pooled results showed that the biallelic mean was not significantly different between PCOS and controls (SMD -. 0.03, 95% CI -. 0.16-0.10, P. =. 0.603), and that the ORs of PCOS were not demonstrated for the individuals with the biallelic mean less than median (OR 0.96, 95% CI 0.68-1.35, P. =. 0.794), with the short CAG allele (OR 0.94, 95% CI 0.80-1.10, P. =. 0.424), or with the X-weighted biallelic mean (OR 0.81, 95% CI 0.46-1.41, P. =. 0.447). Further, as for the relationship between CAG repeat length and T levels in PCOS patients, the biallelic mean was not significantly different between PCOS patients with high T and those with low T (SMD 0.79, 95% CI -. 0.12-1.70, P. =. 0.088), while the summary correlation r indicated that the CAG biallelic mean appeared to be positively associated with T levels in PCOS (r 0.20, 95% CI 0.11-0.30, p. =. 0.000). Conclusions: This meta-analysis demonstrates no evident association between the CAG length variations in AR gene and PCOS risk, while the CAG length appears to be positively associated with T levels in PCOS patients. © 2013 Elsevier B.V.
Jin C.,Rowan University |
Jin C.,Shaoxing Women and Childrens Hospital |
Strich R.,Rowan University |
Cooper K.F.,Rowan University
Molecular Biology of the Cell | Year: 2014
The yeast C-type cyclin represses the transcription of genes required for the stress response and meiosis. To relieve this repression, cyclin C undergoes nuclear-to-cytoplasmic translocation in response to many stressors, including hydrogen peroxide, where it is destroyed by ubiquitin-mediated proteolysis. Before its destruction, cyclin C promotes stress-induced mitochondrial fission and programmed cell death, indicating that relocalization is an important cell fate regulator. Here we show that cyclin C cytoplasmic translocation requires the cell wall integrity (CWI) mitogen-activated protein kinase Slt2p, its pseudokinase paralogue, Kdx1p, and an associating transcription factor, Ask10p. Furthermore, Slt2p and Kdx1p regulate cyclin C stability through different but required mechanisms. Slt2p associates with, and directly phosphorylates, cyclin C at Ser-266. Eliminating or mimicking phosphorylation at this site restricts or enhances cyclin C cytoplasmic translocation and degradation, respectively. Conversely, Kdx1p does not bind cyclin C but instead coimmunoprecipitates with Ask10p, a transcription factor previously identified as a regulator of cyclin C destruction. These results reveal a complex regulatory circuitry involving both downstream effectors of the CWI mitogen-activated protein kinase signal transduction pathway to target the relocalization and consequent destruction of a single transcriptional repressor. © 2014 Hutchins.
Lu Y.-H.,Womens Hospital |
Lu Y.-H.,Shaoxing Women and Childrens Hospital |
Wang N.,Womens Hospital |
Jin F.,Womens Hospital
Journal of Zhejiang University: Science B | Year: 2013
Children conceived via assisted reproductive technologies (ART) are nowadays a substantial proportion of the population. It is important to follow up these children and evaluate whether they have elevated health risks compared to naturally conceived (NC) children. In recent years there has been a lot of work in this field. This review will summarize what is known about the health of ART-conceived children, encompassing neonatal outcomes, birth defects, growth and gonadal developments, physical health, neurological and neurodevelopmental outcomes, psychosocial developments, risk for cancer, and epigenetic abnormalities. Most of the children conceived after ART are normal. However, there is increasing evidence that ART-conceived children are at higher risk of poor perinatal outcome, birth defects, and epigenetic disorders, and the mechanism(s) leading to these changes have not been elucidated. Continuous follow-up of children after ART is of great importance as they progress through adolescence into adulthood, and new ART techniques are constantly being introduced. © 2013 Zhejiang University and Springer-Verlag Berlin Heidelberg.
PubMed | Shaoxing Women and Childrens Hospital
Type: Journal Article | Journal: Gynecological endocrinology : the official journal of the International Society of Gynecological Endocrinology | Year: 2016
To evaluate the possible relationship between subclinical hypothyroidism (SCH) and metabolic syndrome (MS) and the response to clomiphene citrate (CC) stimulation in women with polycystic ovary syndrome (PCOS).One hundred and ninety-six women with PCOS were divided into two groups: (1) the SCH group with 92 patients; (2) the euthyroid (EU) group with 104 patients. Physical characteristics and metabolic parameters as well as the reaction to CC stimulating test were compared between these two groups.(1) In the SCH group, significantly higher body mass index, Ferriman-Gallwey score, serum triglyceride, insulin and glucose of oral glucose tolerance test, homeostatic model assessment-insulin resistance (HOMA-IR) and significantly lower serum high-density lipoprotein cholesterol was observed in comparison with those in the EU group (p<0.05). (2) The prevalence of CC resistance (30.4%), IR (43.5%) and MS (34.8%) in the SCH group was significantly higher than that in the EU group (p < 0.05).SCH was found associated with IR, MS and CC resistance in women with PCOS. PCOS patients with SCH may have a poorer treatment response to ovulation induction with CC.