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Biomedical subjects

Li Yuan

Publications and source records attributed to Li Yuan.

At least 37 records · Page 2Linked to original sources
PubMed2005

Effects of human Na(+)/dicarboxylate cotransporter 3 on the replicative senescence of human embryonic lung diploid fibroblasts.

To investigate the role of human Na(+)/dicarboxylate cotransporter 3 (hNaDC3) in the replicative senescence of normal human embryonic lung diploid fibroblasts (WI-38), a retroviral vector containing hNaDC3 was constructed. hNaDC3 was introduced into normal WI-38 cells through infection with the retroviral virus. Monoclones were selected with G418. The integration and expression of exotic genes were confirmed by Northern blot and Western blot. When compared with the control cells, WI-38 cells transfected with hNaDC3 cDNA showed significant suppression of growth rate (by 40%), increase of positive rate of SA-beta-gal staining, decrease of mitochondrial membrane potential, shortening of telomere length, and increase of P16 and P21 expression. The morphology characteristics of senescent fibroblasts appeared earlier. Our results have, for the first time, demonstrated that high expression of hNaDC3 may be able to, at least partly, promote the cellular senescence of human diploid fibroblasts.

Blotting, Northern↗
PubMed2005

Functional analysis of FP25K of Helicoverpa armigera single nucleocapsid nucleopolyhedrovirus.

The fp25k gene of Helicoverpa armigera single nucleocapsid nucleopolyhedrovirus (HearNPV) was studied. HearNPV fp25k gene transcription was found starting from about 18 h post-infection, and protein could be detected from the same time with antiserum against FP25K. To study the function of HearNPV fp25k, a recombinant HearNPV (HaBacWD11) with an enhanced green fluorescent protein (GFP) gene replacing the fp25k was constructed using HaBacHZ8, a bacmid of HearNPV that lacks the polyhedrin gene. Growth curve analysis showed that HaBacWD11 produced higher titres of budded viruses (BVs) than its wild-type counterpart HaBacHZ8-GFP. Electron microscopic analysis indicated that at the late stage of infection, the number of intranuclear enveloped nucleocapsids in HaBacWD11-infected cells was much less than that of HaBacHZ8-GFP. A rescue recombinant virus HaBacWD14 was constructed by reintroducing fp25k gene into HaBacWD11. The growth curve and electron microscopic analysis of the rescued recombinant confirmed that the increase of BV yield and the decrease of the virion production in infected cells were the result of fp25k deletion. The expression of membrane fusion protein (Ha133) and ODV-E66 were studied using the FP25K mutants HaBacWD11 and HaBacHZ8-GFP. Unlike FP25K mutants in Autographa californica multicapsid NPV (AcMNPV), which caused an increase in the expression of membrane fusion protein GP64 and a decrease of ODV-E66, no obvious changes at the expression level of Ha133 and ODV-E66 were observed in HearNPV FP25K mutant.

Animals↗
PubMed2005

Vascular development: from precursor cells to branched arterial and venous networks.

The adult vascular system is composed of an arterial, a venous and a lymphatic compartment. These different compartments respectively provide oxygen and nutrients to peripheral organs, remove carbon dioxide and waste products and maintain an immune barrier to defend the host against foreign organisms. Malfunctions of the vascular system represent a major cause of mortality and disease in developed countries. Understanding of the molecular mechanisms regulating vascular system development and maintenance is thus crucial for the design of therapies to cure vascular diseases. The molecules implicated in the control of physiological and pathological angiogenesis in the adult already function during embryonic development. Indeed, the survival of the embryo also critically depends on the establishment of a functional circulatory loop. Here we review our current knowledge about the emergence of endothelial precursor cells in the embryo, of their assembly into the primary vascular plexus and of the remodeling of this plexus into arteries and veins. We also focus on the molecular mechanisms controlling the development of arteries, veins and lymphatic vessels.

Animals↗
PubMed2005

[Influences of gonadotropin releasing hormone agonist treatment on nitric oxide synthase expression in women with endometriosis and infertility].

OBJECTIVE: To explore the expression of endothelial and inducible nitric oxide synthase (eNOS and iNOS) in the eutopic endometria of patients with endometriosis and infertility, and to detect the effect of gonadotropin releasing hormone agonist (GnRH-a) therapy on their expressions. METHODS: Immunohistochemistry and Western immunoblot assay were used to screen eNOS and iNOS expression in endometria of patients with stage III to IV endometriosis and infertility without (30 cases, endometriosis group) and with GnRH-a treatment (18 cases, treatment group), and of 19 patients with carcinoma in situ of the cervix (control group). Using electrochemiluminescence immunoassay, serum estradiol (E(2)) or progesterone (P) concentrations were assayed. RESULTS: eNOS was localized predominantly to the endometrial glandular epithelium, luminal epithelium, and microvascular endothelium. iNOS staining was light, and it, when present, was predominantly found in glandular epithelium and stromal cells. By Western immunoblot analysis, iNOS was not detected. During the early-, mid-, and late-proliferative phases, and the early-, mid-, and late-secretory phases, endometrial eNOS protein relative levels were 0.30 +/- 0.04, 0.40 +/- 0.03, 0.49 +/- 0.03, 0.43 +/- 0.04, 0.55 +/- 0.04 and 0.48 +/- 0.03 in endometriosis group, 0.22 +/- 0.03, 0.37 +/- 0.03, 0.45 +/- 0.04, 0.35 +/- 0.05, 0.50 +/- 0.03 and 0.41 +/- 0.00 in treatment group, and 0.21 +/- 0.03, 0.33 +/- 0.03, 0.45 +/- 0.04, 0.40 +/- 0.03, 0.47 +/- 0.05 and 0.41 +/- 0.03 in control group, respectively. Eutopic endometria in endometriosis group showed higher levels of eNOS protein than that of the control group, but a significant difference was found only in early-, mid-proliferative phases and mid-, late-secretory phases (P < 0.05). Compared with endometriosis group, endometrial eNOS levels in treatment group were reduced, but a significant difference was found only in early proliferative phase and early-, mid-secretory phases (P < 0.05). A significant positive correlation was found between serum E(2) or P concentrations and endometrial expression of eNOS (P < 0.01). CONCLUSIONS: The higher endometrial expression of eNOS in patients with stage III to IV endometriosis may be related to the pathogenesis of endometriosis and the associated subfertility. The expression of eNOS is markedly reduced by administration of GnRH-a.

Adult↗
PubMed2004

The netrin receptor UNC5B mediates guidance events controlling morphogenesis of the vascular system.

Blood vessels and nerves are complex, branched structures that share a high degree of anatomical similarity. Guidance of vessels and nerves has to be exquisitely regulated to ensure proper wiring of both systems. Several regulators of axon guidance have been identified and some of these are also expressed in endothelial cells; however, the extent to which their guidance functions are conserved in the vascular system is still incompletely understood. We show here that the repulsive netrin receptor UNC5B is expressed by endothelial tip cells of the vascular system. Disruption of the Unc5b gene in mice, or of Unc5b or netrin-1a in zebrafish, leads to aberrant extension of endothelial tip cell filopodia, excessive vessel branching and abnormal navigation. Netrin-1 causes endothelial filopodial retraction, but only when UNC5B is present. Thus, UNC5B functions as a repulsive netrin receptor in endothelial cells controlling morphogenesis of the vascular system.

Animals↗
PubMed2004

Regulation of insulin secretion and expression of SUR1 gene by chronic exposure to free fatty acids in rat pancreatic beta cells.

To study the effects of free fatty acids on insulin secretion and expression of SUR1 gene in rat pancreatic B cells in vitro, and to explore the molecular mechanisms in lipotoxicity inducing insulin secretion dysfunction, pancreatic islet cells were isolated and digested from male SD rats. Purified islets were incubated with either 0.25 mmol/L palmitate or 0.125 mmol/L oleate for 48 h in vitro. Then islets were stimulated with either 5.6 mmol/L or 16.7 mmol/L glucose for 1 h. Insulin release was measured by using radioimmunoassay, and the expression of SUR1 gene mRNA was quantified by reserve transcription-polymerase chain reaction (RT-PCR). The islets exposed to both palmitate and oleate for 48 h showed an increased basal and a decreased glucose-indused insulin release as compared with control islets. Palmitate increased basal insulin secretion by 110% (P< 0.01), decreased glucose stimulated insulin secretion by 43% (P<0.01); while oleate increased basal insulin secretion by 80% (P<0.01) and decreased glucose stimulated insulin secretion by 32 % (P<0.05). RT-PCR showed that oleate significantly suppressed SUR1 gene expression by 64 % (P<0.01) as compared with the control group, while palmitate group manifested a light decrease of 15% (P>0.05) of SUR1 gene expression. Our results suggested that chronic exposure to free fatty acids of pancreatic beta cells inhibited glucose stimulated insulin secretion. Regulation of SUR1 gene expression may be involved in such effects, which may also be one of the molecular mechanisms in lipotoxocity inducing beta cells secretion dysfunction.

ATP-Binding Cassette Transporters↗
PubMed2004

Accumulation of Pb, Cd, Cu and Zn in plants and hyperaccumulator choice in Lanping lead-zinc mine area, China.

A field survey of higher terrestrial plants growing on Lanping lead-zinc mine, China were conducted to identify species accumulating exceptionally large concentrations of Pb, Cd, Cu and Zn of 20 samples of 17 plant species. Concentrations of Pb and Zn in soil and in plant were higher than that of Cu and Cd. Significant difference was observed among the average concentrations of four heavy metals in plants (except Cd and Cu) and in soil (except Pb and Zn) (P<0.05). For the enrichment coefficient of the four heavy metals in plant, the order of average was Pb tree>herbaceous, and herbaceous grew in soil with the highest concentrations of four heavy metals. In different areas, the concentrations of Pb, Cd, Cu and Zn in plants and soils and enrichment coefficient were different. Plants in Paomaping had more accumulating ability to Pb, Cd and Zn, and plants in Jinfeng River had more accumulating ability to Cu. Six plant species, i.e. S. cathayana, Lithocarpus dealbatus, L. plyneura, Fargesia dura, Arundinella yunnanensis and R. annae in Paomaping, had high accumulation capacity. R. annae in Paomaping had hyperaccumulating capacity to Pb, Cd and Zn, L. plyneura to Pb and Cd, and S. cathayana to Cd, respectively.

China↗
PubMed2004

Synthesis and DNA interaction studies of a binuclear ruthenium(II) complex with 2,9-bis(2-imidazo[4,5-f][1,10]phenanthroline)-1,10-phenanthroline as bridging and intercalating ligand.

A novel binuclear complex [(bpy)2Ru(mu-bipp)Ru(bpy)2](ClO4)4, where bpy=2,2'-bipyridine and bipp=2,9-bis(2-imidazo[4,5-f][1,10]phenanthroline)-1,10-phenanthroline has been synthesized. Photophysical results reveal that this complex interacts with calf-thymus DNA with intrinsic binding constant 2.6 x 10(5) M(-1) in the buffer containing 5 mM Tris and 50 mM NaCl. The fact that the intraligand transition of bipp around 370 nm decreased by up to 50% in the presence of DNA, much more pronounced than the metal to ligand charge transfer band around 445 nm indicates the bridging ligand bipp is also the intercalating ligand into DNA base pairs. The emission band around at 601 nm increased by 1.4-fold, and red shifted 14 nm when DNA was added to saturation. The emission quenching of this complex by K4[Fe(CN)6] was depressed greatly when DNA was present. Viscometric measurements also proved the intercalative binding mode.

Animals↗
PubMed2004

Moclobemide up-regulates proliferation of hippocampal progenitor cells in chronically stressed mice.

AIM: To explore the action mechanism of antidepressants. METHODS: The PC12 cell proliferation was detected by flow cytometry. The proliferation of hippocampal progenitor cells and level of brain-derived neurotrophic factor (BDNF) were measured by immunohistochemistry. RESULTS: Treatment with N-methylaspartate (NMDA) 600 micromol/L for 3 d significantly decreased the percentage of S-phase in PC12 cells, while in the presence of classical antidepressant, moclobemide (MOC) 2 and 10 micromol/L, the percentage in S-phase increased. Furthermore, the proliferation of progenitor cells in hippocampal dentate gyrus (subgranular zone), as well as the level of BDNF in hippocampus significantly decreased in chronically stressed mice, while chronic administration with MOC 40 mg/kg (ip) up-regulated the progenitor cell proliferation and BDNF level in the same time course. CONCLUSION: Up-regulation of the proliferation of hippocampal progenitor cells is one of the action mechanisms for MOC, which may be closely related to the elevation of BDNF level at the same time. These results also extend evidence for our hypothesis that up-regulation of the hippocampal neurogenesis is one of the common mechanisms for antidepressants.

Animals↗
PubMed2003

Flow regulates arterial-venous differentiation in the chick embryo yolk sac.

Formation of the yolk sac vascular system and its connection to the embryonic circulation is crucial for embryo survival in both mammals and birds. Most mice with mutations in genes involved in vascular development die because of a failure to establish this circulatory loop. Surprisingly, formation of yolk sac arteries and veins has not been well described in the recent literature. Using time-lapse video-microscopy, we have studied arterial-venous differentiation in the yolk sac of chick embryos. Immediately after the onset of perfusion, the yolk sac exhibits a posterior arterial and an anterior venous pole, which are connected to each other by cis-cis endothelial interactions. To form the paired and interlaced arterial-venous pattern characteristic of mature yolk sac vessels, small caliber vessels of the arterial domain are selectively disconnected from the growing arterial tree and subsequently reconnected to the venous system, implying that endothelial plasticity is needed to fashion normal growth of veins. Arterial-venous differentiation and patterning are controlled by hemodynamic forces, as shown by flow manipulation and in situ hybridization with arterial markers ephrinB2 and neuropilin 1, which show that expression of both mRNAs is not genetically determined but plastic and regulated by flow. In vivo application of ephrinB2 or EphB4 in the developing yolk sac failed to produce any morphological effects. By contrast, ephrinB2 and EphB4 application in the allantois of older embryos resulted in the rapid formation of arterial-venous shunts. In conclusion, we show that flow shapes the global patterning of the arterial tree and regulates the activation of the arterial markers ephrinB2 and neuropilin 1.

Animals↗
PubMed2003

Cellular and molecular mechanisms of embryonic haemangiogenesis and lymphangiogenesis.

Vascular diseases are the leading cause of morbidity and mortality in developed nations. Therapeutic haemangiogenesis and lymphangiogenesis may present a chance for curative intervention. Recently we have learned that physiologic and pathologic angiogenesis in the human adult are controlled by molecules that are already functioning during embryogenesis, and the lessons we can learn from studying embryos may be useful for future clinical studies. Here we review cellular and molecular mechanisms of embryonic haemangiogenesis and lymphangiogenesis. The focus lies on the endothelial cell and the surrounding peri-endothelial cells, the growth factors and receptors that control their development, proliferation, maintenance, regression and differentiation. Our rapidly expanding knowledge of the molecules expressed in endothelial cells justifies expanded functional studies in future

Animals↗
PubMed2003

Open reading frame 94 of Helicoverpa armigera single nucleocapsid nucleopolyhedrovirus encodes a novel conserved occlusion-derived virion protein, ODV-EC43.

Open reading frame 94 (Ha94) of Helicoverpa armigera single nucleocapsid nucleopolyhedrovirus (HaSNPV) is 1086 bp long and a homologue of Autographa californica multiple NPV ORF109. The gene is conserved among all baculoviruses whose genomes have been completely sequenced so far and is thus considered a baculovirus core gene. Ha94 transcripts were detected from 24 to 96 h post-infection (p.i.) of HzAM1 cells with HaSNPV. Polyclonal antiserum raised to a GST-HA94 fusion protein recognized a 43 kDa protein, HA94, in infected cell lysates from 36 to 96 h p.i., suggesting that Ha94 is a late gene. Western blot analysis of proteins present in budded virus and occlusion-derived virus (ODV) showed that Ha94 encodes a structural component of ODV. When ODVs were fractionated further into nucleocapsid and envelope components, Western blot analysis indicated that the encoded protein was associated with both the nucleocapsid and the envelope. In summary, data available indicated that Ha94 encodes a novel ODV-specific protein of HaSNPV, designated ODV-EC43.

Amino Acid Sequence↗
PubMed2003

A new IL-1 receptor inhibitor 139A: fermentation, isolation, physico-chemical properties and structure.

Interleukin (IL)-1 is known to be a cytokine which plays a major role in pathological conditions like septic shock, inflammation and auto-immune disease, hence, methods that reduce the activity of IL-1 have an impact on clinical medicine. Inhibiting the binding of IL-1 to IL-1 receptors is one of the methods. A new inhibitor of IL-1 receptor, 139A, was isolated from the fermentation broth of Streptomyces sp.139. It was extracted from the broth filtrate, purified by Diaion HP-20, cation exchange resin and DEAE Sephadex A-25. 139A was identified as polysaccharide, its structure was elucidated on the basis of spectral analysis, the immobilized ligand IL-1 receptor binding assay (IL-ILRBA) proved 139A can competitively inhibits the binding of IL-1 to IL-1 receptors.

Chromatography, Gel↗
PubMed2003

Metformin modulates insulin post-receptor signaling transduction in chronically insulin-treated Hep G2 cells.

AIM: To study the effect of chronic insulin treatment on insulin post-receptor signaling transduction and whether the effects of metformin are transmitted throughout the cascade of insulin signaling intermediates in a human hepatoma cell line (Hep G2). METHODS: Hep G2 cells were incubated in serum free media containing either insulin 100 nmol/L or insulin 100 nmol/L plus different concentrations (0.01-10 mmol/L) of metformin for 16 h and then were stimulated with insulin 100 nmol/L for 1 min. RESULTS: Chronic treatment of insulin 100 nmol/L induced a significant reduction in the phosphorylation and protein expression of IR?, IRS1 and IRS2, which therefore resulted in a downregulation of association of PI3K with IRS. Therapeutic concentrations (0.01-0.1 mmol/L) of metformin prevented the changes induced by chronic insulin treatment in these post-receptor components of insulin signaling pathway. Tyrosine phosphorylation of IR?, IRS1, and IRS2 was increased by 2.7 fold (P < 0.01), 6.8 fold (P < 0.01), and 2.3 fold (P <0.01) of chronically insulin-treated cells alone, respectively, after metformin 0.1 mmol/L was added. The association of p85 with IRS1 and IRS2 was also increased from 34 % to 86 % (P <0.01) and from 30 % to 92 % (P <0.01), respectively. In contrast, metformin in pharmacological concentration (1-10 mmol/L) further inhibited tyrosine phosphorylation of IR?, IRS1, IRS2 and the interaction of PI3K with IRS. The association of IRS1 with p85 was further decreased by 58 % (P >0.05) and of IRS2 by 30 % (P <0.05). CONCLUSION: Chronic insulin exposure of Hep G2 cells induces the downregulation of insulin signal transduction via PI3K pathway. The effect of metformin on insulin signaling transduction represent a primary mechanism of metformin action in insulin resistant state.

Carcinoma, Hepatocellular↗
PubMed2003

Regulation of leptin on insulin secretion and sulfonulurea receptor 1 transcription level in isolated rats pancreatic islets.

OBJECTIVE: To investigate the regulation of leptin on insulin secretion and expression of ATP-sensitive potassium channel subunit sulfonulurea receptor 1 (SUR1) mRNA, and to determine whether the effects of leptin are mediated through known intracellular signaling transduction. METHODS: Pancreatic islets were isolated by the collagenase method from male SD rats. The purified islets were incubated with different concentrations of leptin for 2 h in the presence of different concentrations of glucose. Insulin release was measured using radioimmunoassay. Expression of SUR1 mRNA was detected by RT-PCR. RESULTS: In the presence of leptin 2 nmol/L, insulin release was significantly inhibited at either 11.1 or 16.7 mmol/L glucose concentration (both P < 0.05), but insulin release was not altered at glucose of 5.6 mmol/L physiological concentration. The dose-response experiment showed that the maximal effect of leptin on insulin secretion achieved at 2 nmol/L. Exposure of islets to 2 nmol/L leptin induced a significant increase of SUR1 transcription levels by 71% (P < 0.01) at 11.1 mmol/L glucose and by 56% (P < 0.05) at 16.7 mmol/L glucose concentration. Selective phosphatidylinositol 3-kinase (PI 3-kinase) inhibitor wortmannin significantly prevented the leptin effect on insulin secretion and SUR1 mRNA expression. CONCLUSIONS: Regulatory effects of leptin on insulin secretion could be biphasic at different concentrations of glucose and leptin. The stimulatory regulation of SUR1 transcription levels may be mediated through activation of PI 3-kinase pathway, which may be a possible mechanism of leptin in regulating insulin secretion.

Animals↗
PubMed2002

Female germ cell aneuploidy and embryo death in mice lacking the meiosis-specific protein SCP3.

Aneuploidy (trisomy or monosomy) is the leading genetic cause of pregnancy loss in humans and results from errors in meiotic chromosome segregation. Here, we show that the absence of synaptonemal complex protein 3 (SCP3) promotes aneuploidy in murine oocytes by inducing defective meiotic chromosome segregation. The abnormal oocyte karyotype is inherited by embryos, which die in utero at an early stage of development. In addition, embryo death in SCP3-deficient females increases with advancing maternal age. We found that SCP3 is required for chiasmata formation and for the structural integrity of meiotic chromosomes, suggesting that altered chromosomal structure triggers nondisjunction. SCP3 is thus linked to inherited aneuploidy in female germ cells and provides a model system for studying age-dependent degeneration in oocytes.

Aneuploidy↗
PubMed2002

Chronic hyperinsulinism induced down-regulation of insulin post-receptor signaling transduction in Hep G2 cells.

To study the regulatory effect of acute and chronic insulin treatment on insulin post-receptor signaling transduction pathway in a human hepatoma cell line (Hep G2), Hep G2 cells were incubated in the presence or absence of insulin with different concentrations in serum free media for 16 h and then stimulated with 100 nmol/L insulin for 1 min. Protein levels of insulin receptor beta-subunit (IR beta), insulin receptor substrate-1 (IRS-1) and p85 subunit of phosphatidylinositol 3-kinase (PI 3-kinase) were determined in total cell lysates by Western-immunoblot. Phosphorylated proteins IR beta, IRS-1 and interaction of PI 3-kinase with IRS-1 were determined by immunoprecipitation. Results showed that 1-min insulin stimulation rapidly induced tyrosine phosphorylation of IR beta and IRS-1, which in turn, resulting in association of PI 3-kinase with IRS-1. 1-100 nmol/L chronic insulin treatment induced a dose-dependent decrease in the protein level of IR beta and a slight decrease in the protein level of IRS-1. There was a more marked reduction in the phosphorylation of IR beta, IRS-1, reaching a nadir of 22% (P < 0.01) and 15% (P < 0.01) of control levels, respectively, after 16 h treatment with 100 nmol/L insulin. The association between IRS-1 and PI 3-kinase was decreased by 66% (P < 0.01). There was no significant change in PI 3-kinase protein levels. These data suggest that chronic insulin treatment can induce alterations of IR beta, IRS-1 and PI 3-kinase three early steps in insulin action, which contributes significantly to insulin resistance, and may account for desensitization of insulin action.

Carcinoma, Hepatocellular↗