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Biomedical subjects

Ming Xu

Publications and source records attributed to Ming Xu.

At least 91 records · Page 5Linked to original sources
PubMed2004

[Role of cyclin D1 in carcinogenesis of human cells induced by quartz].

OBJECTIVE: To study the role of cyclin D1 in malignant transformation of human embryonic lung diploid fibroblasts (HELF) induced by quartz. METHODS: pXJ41-cyclin D1 expressing sense and antisense cyclin D1 RNA were transinfected into malignant transformed HELF induced by quartz with DNA recombination and gene transduction. The expression of cyclin D1 was detected with hybridization in situ and immunohistochemistry methods to analyze changes in cell growth, double multiplication time, distribution of cell cycles, colony forming ability on soft agar, etc., before and after cyclin D1 transduction. RESULTS: During the process of malignant transformation of HELF induced by quartz, cyclin D1 gene was overexpressed. Antisense pXJ41-cyclin D1 RNA could suppress the growth and proliferation of malignant transformed cells induced by quartz. Growth speed of antisense pXJ41-cyclin D1 transinfected cells decreased by 58.69% on the 8th day in culture, as compared to malignant transformed cells induced by quartz, and its double multiplication time prolonged from 21.0 h to 31.4 h. Antisense cyclin D1 RNA led to cell cycle arrest, resulting in lengthened G1 phase (proportion of cells in phase G1 increased to 52.7% from 45.1% and that of cells in phase S decreased to 33.1% from 40.3%). Colony forming rate reduced significantly and size of colony became smaller. CONCLUSIONS: Abnormal expression of cyclin D1 in cells related to their malignant transformation induced by quartz. Highly expressed cyclin D1 could play an important role in maintaining the transformed phenotype of malignant cells.

Cell Transformation, Neoplastic↗
PubMed2004

[Synthesis of BODIPY-FL-labeled phenylephrine and the determination of its biological activity].

OBJECTIVE: To synthesize BODIPY-FL-labeled phenylephrine (BODIPY-FL-PE) and determine its biological activity. METHODS: Condensation of BODIPY-FL (green fluorescence dye) and phenylephrine (alpha1-adrenoceptor agonist) was performed by adding dicyclohexylcarbodiimide (DCC) in the presence of absolute tetrahydrofuran(THF). The reaction occurred in absolutely oxygen and water condition at room temperature. The crude product was separated and purified by thin-layer chromatography (TLC). The structure of BODIPY-FL-PE was characterized by TLC and mass spectrometry (MS). Its pharmabiological activity was determined by Western blot. RESULTS: BODIPY-FL-PE,the target molecule, was synthesized and its structure was identified by using ultra-violet spectrometry (UV) and MS. The result of Western blot indicated that alpha1-adrenoceptor (alpha1-AR) induced ERK phosphorylation was confirmed in both BODIPY-FL-PE and PE treated groups. CONCLUSION: The synthesized BODIPY-FL-PE has pharmacological activity that could activate alpha1-AR. Visualization of AR behaviors could be achieved by tracing the trajectories of BODIPY-FL-PE labeled AR. It might be a promising tool for investigating dynamic behaviors of AR in living cells.

Adrenergic alpha-1 Receptor Agonists↗
PubMed2003

Endonuclease G is required for early embryogenesis and normal apoptosis in mice.

Endonuclease G (EndoG) is a nuclear-encoded mitochondrial protein reported to be important for both nuclear DNA fragmentation during apoptosis and mitochondrial DNA replication. To evaluate the in vivo function of EndoG, we have investigated the effects of EndoG deficiency in cells and mice. We found that EndoG homozygous mutant embryos die between embryonic days 2.5 and 3.5. Mitochondrial DNA copy numbers in ovulated oocytes from EndoG heterozygous mutant and wild-type mice are similar, suggesting that EndoG is involved in a cellular function unrelated to mitochondrial DNA replication. Interestingly, we found that cells from EndoG heterozygous mutant mice exhibit increased resistance to both tumor necrosis factor alpha- and staurosporine-induced cell death. Moreover, spontaneous cell death of spermatogonia in EndoG heterozygous mutant mice is significantly reduced compared with wild-type mice. DNA fragmentation is also reduced in EndoG+/- thymocytes and splenocytes compared with wild-type cells, as well as in EndoG+/- thymus in vivo compared with that of the wild-type mice, on activation of apoptosis. These findings indicate that EndoG is essential during early embryogenesis and plays a critical role in normal apoptosis and nuclear DNA fragmentation.

Animals↗
PubMed2003

BUBR1 deficiency results in abnormal megakaryopoiesis.

The physiologic function of BUBR1, a key component of the spindle checkpoint, was examined by generating BUBR1-mutant mice. BUBR1(-/-) embryos failed to survive beyond day 8.5 in utero as a result of extensive apoptosis. Whereas BUBR1(+/-) blastocysts grew relatively normally in vitro, BUBR1(-/-) blastocysts exhibited impaired proliferation and atrophied. Adult BUBR1(+/-) mice manifested splenomegaly and abnormal megakaryopoiesis. BUBR1 haploinsufficiency resulted in an increase in the number of splenic megakaryocytes, which was correlated with an increase in megakaryocytic, but a decrease in erythroid, progenitors in bone marrow cells. RNA interference-mediated down-regulation of BUBR1 also caused an increase in polyploidy formation in murine embryonic fibroblast cells and enhanced megakaryopoiesis in bone marrow progenitor cells. However, enhanced megakaryopoiesis in BUBR1(+/-) mice was not correlated with a significant increase in platelets in peripheral blood, which was at least partly due to a defect in the formation of proplatelet-producing megakaryocytes. Together, these results indicate that BUBR1 is essential for early embryonic development and normal hematopoiesis.

Animals↗
PubMed2003

Function of gamma-aminobutyric acid receptor/channel rho 1 subunits in spinal cord.

gamma-Aminobutyric acid (GABA) receptor/channel rho 1 subunits are important components in inhibitory pathways in the central nervous system. However, the precise locations and roles of these receptors in the central nervous system are unknown. We studied the expression localization of GABA receptor/channel rho 1 subunit in mouse spinal cord and dorsal root ganglia (DRG). The immunohistochemistry results indicated that GABA receptor/channel rho 1 subunits were expressed in mouse spinal cord superficial dorsal horn (lamina I and lamina II) and in DRG. To understand the functions of the GABA receptor/channel rho 1 subunit in these crucial sites of sensory transmission in vivo, we generated GABA receptor/channel rho 1 subunit mutant mice (rho 1-/-). GABA receptor/channel rho 1 subunit expression in the rho 1-/- mice was eliminated completely, whereas the gross neuroanatomical structures of the rho 1-/- mice spinal cord and DRG were unchanged. Electrophysiological recording showed that GABA-mediated spinal cord response was altered in the rho 1-/- mice. A decreased threshold for mechanical pain in the rho 1-/- mice compared with control mice was observed with the von Frey filament test. These findings indicate that the GABA receptor/channel rho 1 subunit plays an important role in modulating spinal cord pain transmission functions in vivo.

Animals↗
PubMed2003

Effect of Gosha-jinki-gan (Chinese herbal medicine: Niu-Che-Sen-Qi-Wan) on insulin resistance in streptozotocin-induced diabetic rats.

Gosha-jinki-gan (GJG) is a Chinese herbal medicine that is known to be useful for the treatment of diabetic neuropathy. In the present study, the effect of GJG on insulin resistance in streptozotocin (STZ, 50 mgkg(-1) BW, i.v.) -induced diabetic rats was examined by means of the euglycemic clamp procedure. To accomplish this objective, diabetic and non-diabetic control rats were divided as follows: a single dose administration of GJG (800 mgkg(-1) BW, p.o.), saline (5 mlkg(-1) BW, p.o.), and GJG (p.o)+N(G)-monomethyl-L-arginine (L-NMMA, 1 mgkg(-1)min(-1) BW, i.v.). In diabetic rats, the incremental area (DeltaAUC [area under curve]) of the glucose metabolic clearance rate (MCR) during a 3.0 mUkg(-1)min(-1) insulin infusion rate was significantly higher in the GJG-administrated group compared to the saline-administrated one. On the other hand, the effect of GJG on the DeltaAUC of MCR in diabetic rats was abolished by L-NMMA. In addition, no significant differences in the DeltaAUC of MCR were observed in non-diabetic control rats. These results suggest that a single dose administration of GJG can improve the glucose utilization and insulin resistance in STZ-induced diabetic rats, probably via the nitric oxide (NO) pathway.

Animals↗
PubMed2003

Altered feeding responses in mice with targeted disruption of the dopamine-3 receptor gene.

Dopamine signaling has been implicated in the control of food intake and body weight. In particular, dopamine is important in the control of meal size and number and is thought to mediate the response to metabolic deprivation states. In the present experiments, the authors assessed the role of the dopamine-3 receptor (D3R) in the feeding responses to 2-deoxy-D-glucose, mercaptoacetate, and peripheral insulin. All 3 compounds increased food intake in wild-type mice, but the hyperphagic responses were blunted in D3R-/- mice. In other experiments, D3R-/- mice were hyperresponsive to the administration of amylin and leptin relative to wild-type mice. These results support the hypothesis that D3Rs chronically inhibit the effects of adiposity hormones, thereby contributing to a net anabolic state.

Animals↗
PubMed2003

7-OH-DPAT and PD 128907 selectively activate the D3 dopamine receptor in a novel environment.

The D3 dopamine receptor is expressed primarily in limbic brain areas, and appears to play an inhibitory role in rodent locomotor behavior. Evidence suggests a potential role for the D3 receptor in the pathology of neuropsychiatric disease. Progress in elucidating D3 receptor function has been hampered, however, by a lack of well-characterized, selective ligands and by conflicting information regarding the behavioral phenotype of D3 receptor knockout mice. Here, we describe studies evaluating the behavioral effects of (+/-)-7-hydroxy-N,N-di-n-propyl-2-aminotetralin (7-OH-DPAT) and PD 128907, two D3 receptor agonists whose in vivo selectivity has been a topic of considerable controversy. We demonstrate that both compounds inhibit locomotion under novel environmental conditions in wild-type (WT) mice, but are without measurable behavioral effect under identical conditions in D3 receptor knockout mice. Additionally, we demonstrate that at low, D3 selective doses, these compounds are without behavioral effect in both WT and D3 receptor knockout mice that have acclimated to the testing environment. These findings suggest that D3 receptor stimulation inhibits novelty-stimulated locomotion, and establish conditions for the use of 7-OH-DPAT and PD 128907 as D3 receptor agonists in vivo. Potential implications of these observations are discussed.

Animals↗
PubMed2003

Ethanol consumption in mice with a targeted disruption of the dopamine-3 receptor gene.

Considerable evidence suggests that the mesolimbic dopaminergic system is an important substrate for the rewarding effects of ethanol consumption. Previous data have demonstrated that pharmacological agents that alter dopamine signaling also influence the self-administration of ethanol. The present experiments were designed to assess the role of the dopamine-3 receptor (D3-R) on voluntary ethanol consumption in C57BL/6 mice. Mice with targeted disruption of the D3-R gene (D3-R - /-) were compared to wild-type controls in an ethanol intake paradigm. In Experiment 1, mice had 24-hour access to ethanol each day in a two-bottle choice paradigm for a period of 7 days per concentration. The concentrations tested were 3, 6, 10 and 15%. In Experiment 2, mice had I hour of access to ethanol each day in a two-bottle paradigm for a period of 7 days per concentration. The same concentrations in Experiment I were compared in Experiment 2. In Experiment 3 we sought to test the development of a conditioned taste aversion (CTA) after receiving an intraperitoneal (ip.) injection of 2.0 g/kg ethanol. In Experiment 4, blood ethanol levels where assessed following a 2.0 g/kg ip.injection of ethanol. Experiment 5 assessed taste preference for saccharine and quinine in wild-type and D3-R -/- mice. Contrary to our predictions, both D3-R -/- and wild-types on a CS57BL/6 background had similar intakes of ethanol, at all concentrations tested, in the 24-hour and 1-hour intake paradigms. Wild-type and D3-R -/- mice respond to injected ethanol similarly by developing a conditioned taste aversion. Metabolic analysis revealed mutant mice are slower in metabolizing a bolus injection of ethanol. Lastly, wild-type and D3-R -/- mice showed similar consumption to increasing concentration of both sweet and bitter tastes. These data suggest that deletion of the D3-R gene does not increase ethanol consumption above that found on the C57BL/6 genetic background. Furthermore, the D3-R -/- mice adequately learn a CTA to ethanol and do not ham differing taste reactivity to saccharin or quinine. However, D3-R -/- mice do appear to have a slower rate of ethanol metabolism.

Alcohol Drinking↗
PubMed2003

[Recombination and identification of sense and antisense cyclinD1 eukaryotic expression vectors].

The exogenous gene cyclinD1 cDNA was inserted into eukaryotic expression vector pXJ41-neo by gene transduction and recombination techniques. The recombinant was detected by electrophoresis. Results showed that the recombinant sense plasmid (pXJ41-cyclinD1) was digested by HindIII into 229 bp, 427 bp and 7554 bp; while the recombinant antisense plasmid was digested into 427 bp, 1184 bp and 6599 bp, implying that sense and antisense pXJ41-cyclinD1 eukaryotic expression vectors were successfully recombined. The finding from this study offers an effective tool to reveal the mechanism of the carcinogenesis of environmental and occupational hazards.

Antisense Elements (Genetics)↗
PubMed2003

[Expression of type II collagen gene and structural change in bone tissues of rats with experimental fluorosis].

OBJECTIVE: To investigate the effects of excessive intake of fluoride on the expression of type II collagen gene and types and morphological change of collagen fiber in the bone tissues of rats. METHODS: A rat model with fluorosis was established by adding 221 mg/L of sodium fluoride (NaF) to drinking water for the rats for 15 days, 30 days and two months, respectively. Type II collagen alpha1 (II) cDNA probe was prepared, and cDNA-mRNA in-situ hybridization was employed to detect change in expression of type II collagen mRNA in the bone tissues of rats with excessive intake of fluoride (221 mg/L NaF). Picrosirius-polarization method was used to observe types of collagen and morphology of collagen fiber in the bone tissues. RESULTS: Chondroblasts were found in the femur and other bone tissues of the rats after exposure to fluoride. cDNA-mRNA in-situ hybridization showed that expression of type II collagen gene could be observed in the cytoplasm of chondrocytic lacuna and chondrified bone tissues. mRNA in collagen of chondrocytes of the rib cartilage reached the peak level 15 days after exposure to fluoride, and decreased gradually one month and two months after exposure. Polychromatic type II collagen, breakage of collagen fiber, disorder array and reduced content of type II collagen could be found in the bone tissues with picrosirius-polarization method. CONCLUSIONS: Excessive intake of fluoride could lead to changes in types and structure of collagen (cross-linkage) of bone tissues, which caused expression of type II collagen gene in the chondrified bone tissues and enhanced its expression in the rib cartilage tissues.

Animals↗
PubMed2003

[Cloning of differentially displayed cDNAs involved in NaF-treated osteoblasts].

OBJECTIVE: To explore the effects of excessive fluoride on the gene expression of rat osteoblasts. METHODS: Rat osteoblasts were treated with 2.0 mmol/L of sodium fluoride (NaF) for two weeks in vitro, and difference in the gene expression between the NaF-treated and normal osteoblasts was compared with mRNA differential display (DD-PCR) technique. RESULTS: Among the six differentially expressed gene fragments which had been cloned, expression of the ribosomal protein L5 gene, ATPase Na(+)K(+) transporting beta polypeptide 3 gene, karyopherin alpha 2 gene and cis-Golgi body p28 gene was lower and expression of ubiquitous-conjugating enzyme E2D 3 gene and a newly-discovered gene fragment in this study showed up-regulated in the NaF-treated osteoblasts of the rats. CONCLUSIONS: Expression of genes changed in the osteoblasts after treatment with fluoride for two weeks and most of them associated with synthesis, transportation and processing of protein. It suggested that excessive fluoride could affect the protein synthesis in osteoblasts by changing the expression of the related genes. A novel gene related to excessive fluoride exposure was also found.

Animals↗
PubMed2003

[Comparison of the mucociliary transport rate of rhinitis sicca and atrophic rhinitis].

OBJECTIVE: To study the mucociliary transport function of rhinitis sicca and atrophic rhinitis, and to explore the standard of diagnosis. METHOD: The MTR of normal control group, the rhinitis sicca group and the atrophic rhinitis were determined by using saccharin, and then compared. Then MTR of rhinitis sicca treatment group were compared before and after treatment. RESULT: The MTR of normal group: (9.15 +/- 0.86) mm/min; the rhinitis sicca group: (5.84 +/- 0.48) mm/min and the atrophic rhinitis group: (3.36 +/- 0.07) mm/min. There were significant difference among them (P < 0.05). 25 patients of rhinitis sicca were treated by administering the pill of Gelomyrtol forte in 2 weeks. The MTR of rhinitis sicca were no significant difference before and after treatment (P > 0.05). CONCLUSION: Rhinitis sicca is a separate nasal disease, which is different from atrophic rhinitis. It is important to find an effective treatment for the disease.

Adolescent↗
PubMed2002

C-fos-deficient mouse hippocampal CA3 pyramidal neurons exhibit both enhanced basal and kainic acid-induced excitability.

Excitotoxicity is a process in which glutamate or other excitatory amino acids induce neuronal cell death. To address whether and how c-fos is involved in neuronal excitotoxicity, we previously generated mice in which the c-fos expression is eliminated specifically in the hippocampus. We found that these mutant mice exhibit increased kainic acid (KA)-induced seizure severity, increased neuronal excitability as measured by electroencephalogram, and increased neuronal cell death compared to wild-type control mice. To further assess the role of c-fos in regulating neuronal excitability at a cellular level, we performed hippocampal slice recording in the current study. We found that c-fos-deficient CA3 pyramidal neurons exhibit both enhanced basal and KA-induced excitability compared to normal control neurons. Our results suggest that c-fos regulates CA3 neuronal excitability.

Animals↗