Key Laboratory of Animal Models and Human Disease Mechanisms

Laboratory of, China

Key Laboratory of Animal Models and Human Disease Mechanisms

Laboratory of, China
SEARCH FILTERS
Time filter
Source Type

Liu H.,Key Laboratory of Animal Models and Human Disease Mechanisms | Zhao B.,State Key Laboratory of Genetic Resources and Evolution | Zhao B.,University of Chinese Academy of Sciences | Chen Y.,CAS Kunming Institute of Zoology | And 7 more authors.
FASEB Journal | Year: 2013

Defects in multiple coagulation factor deficiency protein 2 (MCFD2) are a cause of factor V and factor VIII combined deficiency type 2 (F5F8D). MCFD2 was also suggested to play an important role as an autocrine/paracrine factor in maintaining neural stem cell potential. The current work provided direct evidence that both amphibian and human MCFD2 can maintain stem cell pluripotency or stemness of rhesus monkey embryonic stem cells (rESCs) as basic fibroblast growth factor 2 (FGF-2) does. In most cases, MCFD2 had identical effects on stem cells as FGF-2. We investigated the possible mechanism of MCFD2 to support stem cell pluripotency by highlighting the effects of MCFD2 and FGF-2 on several signaling pathways in rESCs, namely MAPK, TGF, Wnt, and Akt, and 3 core transcriptional factors (Oct4, Nanog, and Sox2). In addition, some features of signaling pathways (MAPK and Akt), which are different from human embryonic stem cells (hESCs) and mouse embryonic stem cells (mESCs), are found in rESCs, indicating that primate ESCs have unique signaling mechanisms. These results may shed light on the biological roles of MCFD2, the conserved protein family distributed in both vertebrates and invertebrates. The ability to support stem cell self-renewal may be the general function of the conserved protein family. © FASEB.


PubMed | Key Laboratory of Animal Models and Human Disease Mechanisms
Type: Journal Article | Journal: Hippocampus | Year: 2010

The formation of memory is believed to depend on experience- or activity-dependent synaptic plasticity, which is exquisitely sensitive to psychological stress since inescapable stress impairs long-term potentiation (LTP) but facilitates long-term depression (LTD). Our recent studies demonstrated that 4 days of opioid withdrawal enables maximal extents of both hippocampal LTP and drug-reinforced behavior; while elevated-platform stress enables these phenomena at 18 h of opioid withdrawal. Here, we examined the effects of low dose of morphine (0.5 mg kg(-1), i.p.) or the opioid receptor antagonist naloxone (1 mg kg(-1), i.p.) on synaptic efficacy in the hippocampal CA1 region of anesthetized rats. A form of synaptic depression was induced by low dose of morphine or naloxone in rats after 18 h but not 4 days of opioid withdrawal. This synaptic depression was dependent on both N-methyl-D-aspartate receptor and synaptic activity, similar to the hippocampal long-term depression induced by low frequency stimulation. Elevated-platform stress given 2 h before experiment prevented the synaptic depression at 18 h of opioid withdrawal; in contrast, the glucocorticoid receptor (GR) antagonist RU38486 treatment (20 mg kg(-1), s.c., twice per day for first 3 days of withdrawal), or a high dose of morphine reexposure (15 mg kg(-1), s.c., 12 h before experiment), enabled the synaptic depression on 4 days of opioid withdrawal. This temporal shift of synaptic depression by stress or GR blockade supplements our previous findings of potentially correlated temporal shifts of LTP induction and drug-reinforced behavior during opioid withdrawal. Our results therefore support the idea that stress experience during opioid withdrawal may modify hippocampal synaptic plasticity and play important roles in drug-associated memory. (c) 2009 Wiley-Liss, Inc.

Loading Key Laboratory of Animal Models and Human Disease Mechanisms collaborators
Loading Key Laboratory of Animal Models and Human Disease Mechanisms collaborators