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Molecular determinants of blastocyst competency for implantation
Haibin Wang 한국발생생물학회 2011 한국발생생물학회 학술발표대회 Vol.30 No.-
Early pregnancy loss in humans, which often occurs due to defects that occur before, during or immediately after implantation, is a worldwide social and economic concern. For successful implantation to occur in the receptive uterus, the blastocyst must also attain implantation competency. The first evidence that the state of activity of the blastocyst determines the “window” of implantation in the receptive uterus was derived from reciprocal blastocyst transfer experiments in a delayed implantation mouse model. This model is a powerful approach to define the molecular signaling components that direct blastocyst activation or dormancy. Nearly 100 mammals in seven different orders undergo delayed implantation, but the underlying mechanism remains largely unknown. There is evidence that catecholestrogens produced from primary estrogens in the uterus activate blastocysts. Another lipid signaling molecule that targets blastocysts is an endocannabinoid anandamide, which activates G-protein coupled cannabinoid receptors CB1 and CB2. Expression of CB1 in the Tr, and uterine synthesis of anandamide, suggest that endocannabinoid signaling is critical to implantation in mice. Levels of uterine anandamide and blastocyst CB1 are coordinately downregulated with the attainment of uterine receptivity and blastocyst activation, respectively, in contrast to their elevated levels in the nonreceptive uterus and dormant blastocysts. Anandamide regulates blastocyst function by differentially modulating MAPK signaling and Ca2+channelactivityviaCB1. Using delayed implantation model, a global gene expression study showed that these two different physiological states of the blastocyst are molecularly distinguishable. The main functional categories of altered genes include cell cycle, cell signaling and energy metabolic pathways. This study also showed an upregulated expression of heparin-binding EGF-like growth factor (HB-EGF) in activated blastocysts and is complementary to earlier reports of upregulated expression of its receptor ErbB1 and ErbB4 in similar blastocysts. Recently, we demonstrated that silencing of Wnt-beta-catenin signaling in mice does not adversely affect the development of preimplantation embryos to blastocysts and uterine preparation for receptivity, but, remarkably, blocks blastocyst competency to implantation. A coordinated activation of canonical Wnt-beta-catenin signaling with Cox-2-PPARd signaling pathway ensures blastocyst competency to implantation. These findings constitute novel evidence that Wnt signaling is at least one pathway that determines blastocyst competency for implantation. More insight into the molecular basis of blastocyst competency for implantation might help to improve pregnancy rates in human IVF programs.
Anxin Wang,Haibin Li,Jinhuan Yuan,Yingting Zuo,Yijun Zhang,Shouhua Chen,Shouling Wu,Yongjun Wang 대한뇌졸중학회 2020 Journal of stroke Vol.22 No.1
Background and Purpose Previous studies suggested increased visit-to-visit variability of total cholesterol (TC) is associated with stroke. This study aimed to investigate the associations of various lipids measurements variability and the risk of stroke and stroke type (ischemic and hemorrhagic stroke). Methods Fifty-one thousand six hundred twenty participants in the Kailuan Study without history of myocardial infarction, stroke, and cancer who underwent three health examinations during 2006 to 2010 were followed for incident stroke. Variability in TC, triglycerides, high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C) measurements were measured using the coefficient of variation (CV), standard deviation (SD), variability independent of the mean (VIM), and average real variability (ARV). Results During a median of 6.04 years of follow-up, 1,189 incident stroke (1,036 ischemic and 160 hemorrhagic stroke) occurred. In the multivariable-adjusted model, the hazard ratio (HR) comparing participants in the highest versus lowest quartile of CV of HDL-C were 1.21 (95% confidence interval [CI], 1.02 to 1.45; P for trend=0.013) for ischemic stroke. The highest quartile of CV of LDL-C was associated with 2.17-fold risk of hemorrhagic stroke (HR, 2.17; 95% CI, 1.25 to 3.75; P for trend=0.002) compared with the lowest quartile. We did not observe any significant association between TC and triglycerides variability with any of stroke. Consistent results were obtained when calculating variability index using SD, VIM, or ARV. Conclusions These findings suggest the high visit-to-visit HDL-C and LDL-C variability were associated with an increased incidence of ischemic and hemorrhagic stroke, respectively.
Wang, Shuaifei,Li, Fangyuan,Qiao, Ruirui,Hu, Xi,Liao, Hongwei,Chen, Lumin,Wu, Jiahe,Wu, Haibin,Zhao, Meng,Liu, Jianan,Chen, Rui,Ma, Xibo,Kim, Dokyoon,Sun, Jihong,Davis, Thomas P.,Chen, Chunying,Tian, American Chemical Society 2018 ACS NANO Vol.12 No.12
<P>Ferroptosis, an iron-based cell-death pathway, has recently attracted great attention owing to its effectiveness in killing cancer cells. Previous investigations focused on the development of iron-based nanomaterials to induce ferroptosis in cancer cells by the up-regulation of reactive oxygen species (ROS) generated by the well-known Fenton reaction. Herein, we report a ferroptosis-inducing agent based on arginine-rich manganese silicate nanobubbles (AMSNs) that possess highly efficient glutathione (GSH) depletion ability and thereby induce ferroptosis by the inactivation of glutathione-dependent peroxidases 4 (GPX4). The AMSNs were synthesized <I>via</I> a one-pot reaction with arginine (Arg) as the surface ligand for tumor homing. Subsequently, a significant tumor suppression effect can be achieved by GSH depletion-induced ferroptosis. Moreover, the degradation of AMSNs during the GSH depletion contributed to <I>T</I><SUB>1</SUB>-weighted magnetic resonance imaging (MRI) enhancement as well as on-demand chemotherapeutic drug release for synergistic cancer therapy. We anticipate that the GSH-depletion-induced ferroptosis strategy by using manganese-based nanomaterials would provide insights in designing nanomedicines for tumor-targeted theranostics.</P> [FIG OMISSION]</BR>
Zhang, Haibin,Zhang, Jing,Wang, Haiyong,Su, Xingyun,Teng, Lisong Asian Pacific Journal of Cancer Prevention 2015 Asian Pacific journal of cancer prevention Vol.16 No.16
Omega-3 polyunsaturated fatty acids (${\omega}$-3 PUFAs) are essential nutrients for human beings and their potential roles against cancer development and progression have become of wide concern recently. Some studies have suggested that perioperative supplementation with omega-3 fatty acids may have beneficial effects in gastrointestinal cancer patients undergoing surgery, while other researchers reported contrary results. This paper reviews recent research to establish therapeutic effects as well as possible underlying mechanisms of ${\omega}$-3 PUFA actions, and to help explain possible reasons for inconsistent results from different institutions.
Jian Fu,Haibin Sun,Yongzhe Zhang,Wei Xu,Chuan Wang,Yanwei Fang,Jianhui Zhao 한국식품영양과학회 2018 Journal of medicinal food Vol.21 No.1
Luteolin (LU) is a widely distributed flavonoid with multitarget effects. The objective of this study was to determine whether LU could reduce the ischemia–reperfusion injury of the spinal cord (SCII) in a rat model. Forty-eight rats were divided into four groups: sham, SCII, SCII+L-LU (50 mg/kg), and SCII+H-LU (100 mg/kg). Abdominal aortic occlusion was carried out for 40 min in all groups. Hindlimb motor functions were evaluated using the Tarlov scoring system. Nissl and terminal deoxynucleotidyl transferase-mediated dUTP biotin nick end labeling (TUNEL) staining were used to detect cell survival and apoptosis in the spinal cord. Spinal cord samples were taken for determination of malondialdehyde, xanthine oxidase, superoxide dismutase, and glutathione peroxidase activities. The levels of tumor necrosis factor-α, interleukin (IL)-1β, and IL-18 were assessed using ELISA kits to examine the inflammatory responses in the spinal cord. Western blot analysis was used to examine the expression of nuclear factor erythroid 2-related factor (Nrf2) and nod-like receptor pyrin domain-containing 3 protein (NLRP3) levels. We found that LU pretreatment significantly improved the locomotor function of rats after SCII, increased neuron survival, and inhibited apoptosis in the spinal cord. Furthermore, the oxidative stress and inflammatory response were significantly suppressed upon treatment with LU. Finally, LU upregulated Nrf2 levels and downregulated NLRP3 protein expression in SCII tissues. Thus, LU exhibited a neuroprotective effect following SCII by alleviating oxidative stress and inhibiting inflammatory responses and cell apoptosis. The possible mechanism may be related to the activation of Nrf2 and inhibition of NLRP3 inflammasome pathway.
Uterine disorders and pregnancy complications: insights from mouse models
Lim, Hyunjung Jade,Wang, Haibin American Society for Clinical Investigation 2010 The Journal of clinical investigation Vol.120 No.4
<P>Much of our knowledge of human uterine physiology and pathology has been extrapolated from the study of diverse animal models, as there is no ideal system for studying human uterine biology in vitro. Although it remains debatable whether mouse models are the most suitable system for investigating human uterine function(s), gene-manipulated mice are considered by many the most useful tool for mechanistic analysis, and numerous studies have identified many similarities in female reproduction between the two species. This Review brings together information from studies using animal models, in particular mouse models, that shed light on normal and pathologic aspects of uterine biology and pregnancy complications.</P>