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Articles by L Cui
Total Records ( 6 ) for L Cui
  D Han , Y Ding , S. L Liu , G Wang , I. C Si , X Wang , L Cui and D. Huang

Fas ligand (FasL) may play an important role in maintaining the immune privilege of intervertebral disc (IVD). Besides, it is closely related to the apoptosis of degenerative disc cells. Nowadays, lots of reports have described about the paradoxical effects of FasL, although the effect of FasL on IVD cells is still under debate. In this study, we tried to investigate the effects of FasL on Fas expression and on the apoptosis of nucleus pulposus (NP) cells in Sprague–Dawley rats. The results showed that the expression of Fas in NP cells was significantly increased by the recombinant FasL. Meanwhile, the apoptosis of NP cells increased markedly in a FasL dose-dependent manner. Interestingly, RNA interference results indicated that the increase of Fas expression and the NP cell apoptosis described previously were inhibited by Fas siRNA, suggesting that RNA interference might be one of novel strategies to prevent IVD cells from apoptosis.

  R. W Gelling , P. M Vuguin , X. Q Du , L Cui , J Romer , R. A Pederson , M Leiser , H Sorensen , J. J Holst , C Fledelius , P. B Johansen , N Fleischer , C. H. S McIntosh , E Nishimura and M. J. Charron

In addition to its primary role in regulating glucose production from the liver, glucagon has many other actions, reflected by the wide tissue distribution of the glucagon receptor (Gcgr). To investigate the role of glucagon in the regulation of insulin secretion and whole body glucose homeostasis in vivo, we generated mice overexpressing the Gcgr specifically on pancreatic β-cells (RIP-Gcgr). In vivo and in vitro insulin secretion in response to glucagon and glucose was increased 1.7- to 3.9-fold in RIP-Gcgr mice compared with controls. Consistent with the observed increase in insulin release in response to glucagon and glucose, the glucose excursion resulting from both a glucagon challenge and intraperitoneal glucose tolerance test (IPGTT) was significantly reduced in RIP-Gcgr mice compared with controls. However, RIP-Gcgr mice display similar glucose responses to an insulin challenge. β-Cell mass and pancreatic insulin content were also increased (20 and 50%, respectively) in RIP-Gcgr mice compared with controls. When fed a high-fat diet (HFD), both control and RIP-Gcgr mice developed similar degrees of obesity and insulin resistance. However, the severity of both fasting hyperglycemia and impaired glucose tolerance (IGT) were reduced in RIP-Gcgr mice compared with controls. Furthermore, the insulin response of RIP-Gcgr mice to an IPGTT was twice that of controls when fed the HFD. These data indicate that increased pancreatic β-cell expression of the Gcgr increased insulin secretion, pancreatic insulin content, β-cell mass, and, when mice were fed a HFD, partially protected against hyperglycemia and IGT.

  C Bauchart Thevret , L Cui , G Wu and D. G. Burrin

Arginine is an indispensable amino acid in neonates and is required for growth. Neonatal intestinal epithelial cells (IEC) are capable of arginine transport, catabolism, and synthesis and express nitric oxide (NO) synthase to produce NO from arginine. Our aim was to determine whether arginine directly stimulates IEC growth and protein synthesis and whether this effect is mediated via mammalian target of rapamycin (mTOR) and is NO-dependent. We studied neonatal porcine IEC (IPEC-J2) cultured in serum- and arginine-free medium with increasing arginine concentrations for 4 or 48 h. Our results show that arginine enhances IPEC-J2 cell survival and protein synthesis, with a maximal response at a physiological concentration (0.1–0.5 mM). Addition of arginine increased the activation of mTOR, p70 ribosomal protein S6 (p70 S6) kinase, and eukaryotic initiation factor 4E-binding protein 1 (4E-BP1) in a time- and dose-dependent manner. The arginine-induced protein synthesis response was not inhibited by the NO inhibitors nitro-l-arginine methyl ester (l-NAME) and aminoguanidine, despite inducible NO synthase expression in IPEC-J2 cells. Moreover, protein synthesis was not increased or decreased in some cases by addition of an NO donor (S-nitroso-N-acetylpenicillamine), arginine precursors (proline and citrulline) in the absence of arginine, or insulin; S-nitroso-N-acetylpenicillamine suppressed phosphorylation of mTOR, p70 S6 kinase, and 4E-BP1. We found a markedly higher arginase activity in IPEC-J2 cells than in primary pig IEC. Furthermore, mTOR inhibition by rapamycin partially (42%) reduced the arginine-induced protein synthesis response and phosphorylation of mTOR and 4E-BP1. We conclude that arginine-dependent cell survival and protein synthesis signaling in IPEC-J2 cells are mediated by mTOR, but not by NO.

  J Angst , L Cui , J Swendsen , S Rothen , A Cravchik , R. C Kessler and K. R. Merikangas

There is growing clinical and epidemiologic evidence that major mood disorders form a spectrum from major depressive disorder to pure mania. The authors examined the prevalence and clinical correlates of major depressive disorder with subthreshold bipolarity compared with pure major depressive disorder in the National Comorbidity Survey Replication (NCS-R).


The NCS-R is a nationally representative face-to-face household survey of the U.S. population conducted between February 2001, and April 2003. Lifetime history of mood disorders, symptoms, and clinical indicators of severity were collected using version 3.0 of the World Health Organization's Composite International Diagnostic Interview.


Nearly 40% of study participants with a history of major depressive disorder had a history of subthreshold hypo-mania. This subgroup had a younger age at onset, more episodes of depression, and higher rates of comorbidity than those without a history of hypomania and lower levels of clinical severity than those with bipolar II disorder.


These findings demonstrate heterogeneity in major depressive disorder and support the validity of inclusion of subthreshold mania in the diagnostic classification. The broadening of criteria for bipolar disorder would have important implications for research and clinical practice.

  Y Yang , X Li , L Cui , M Fu , A. B Rabie and D. Zhang

Mechanical stress induces human periodontal ligament (PDL) cells to express an osteoblastic phenotype in vitro. Core binding factor a1 (CBFA1) is a key regulator of osteoblast differentiation. This study was designed to investigate the role of CBFA1 in alveolar bone remodelling, specifically the expression of CBFA1 messenger RNA (mRNA) in human PDL cells under mechanical stress and its up- and downstream relationships with other bone remodelling markers. Cultured human PDL cells were exposed to mechanical stress. The expressions of CBFA1 and alkaline phosphatase (ALP), osteopontin (OPN), osteoprotegrin (OPG), and receptor activator nuclear factor kappa B ligand (RANKL) were detected before and after RNA interference (RNAi) of CBFA1. The data were analysed using a t-test and one-way analysis of variance.

After mechanical stress loading, CBFA1 mRNA expression was raised initially, followed by an increased expression of ALP and RANKL, decreased expression of OPG, and a change in OPN expression. After CBFA1 knock-down in human PDL cells by small hairpin (sh) RNA, the expression of ALP, OPN, OPG, and RANKL also changed. These findings suggest that in the present model system CBFA1 may play an important role in PDL-mediated bone remodelling in response to mechanical stimulation. Mechanical stress: CBFA1–ALP and OPG–PDL homeostasis may be one of the signal transduction pathways of human PDL cell differentiation under mechanical stress without exclusion of the involvement of other pathways.

  X Xi , L Cui and W. He

The crystal structure analysis demonstrated that the hydrophobic amino acid residue (isolecuine/leucine/valine) at conserved position 97 of V2 TCR plays an important role in recognizing the non-peptide antigen. But its importance to protein antigen remains unclear until now. In the present study, we focus on the role of hydrophobic amino acid residue at conserved position 97 of V2 TCR in complementarity determining region (CDR)3-mediated binding to protein antigen. We employed CDR3 peptide and membrane-engineered TCR as detecting molecules with mutated 97 hydrophobic amino acid residue in CDR3 (nominated as OT10), a V2 CDR3 sequence derived from tumor infiltrating lymphocytes in ovarian epithelial carcinoma (OEC). Binding assays revealed that OT10 peptide and membrane-engineered TCR ( TCR transfected cells with OT10 sequence) could bind specifically ovarian tumor cell line (SKOV3). The mutant analysis indicated that any amino acid substitution at position I97 could abolish the response of the transfected cells to iso-butylamine, a known non-peptide antigen of T cells. But amino acid substitution of isoleucine at position 97 did not change the responsiveness of TCR transfected cell to protein antigen. Our data suggested that a mechanism other than non-peptide antigen might mediate the recognition of V2 T cells for protein antigen. This finding may provide a possibility that TCR recognize different ligands in diversity manners.

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