Biomedical subjects

Ming-Jie Wang

Publications and source records attributed to Ming-Jie Wang.

6 recordsLinked to original sources

PubMed2006

A Semliki Forest virus replicon vectored DNA vaccine expressing the E2 glycoprotein of classical swine fever virus protects pigs from lethal challenge.

Classical swine fever virus (CSFV) causes significant losses in pig industry in many countries in Asia and Europe. The E2 glycoprotein of CSFV is the main target for neutralizing antibodies. Recently, the replicon of alphaviruses, such as Semliki Forest virus (SFV), has been developed as replicative expression vectors for gene delivery. In this study, we constructed a plasmid DNA based on SFV replicon encoding the E2 glycoprotein of CSFV and evaluated its efficacy in rabbits and pigs. The results showed that the animals immunized with the DNA vaccine developed CSFV-specific neutralizing antibodies and were protected from virulent or lethal challenge. This demonstrates that the SFV replicon-derived DNA vaccine can be a potential marker vaccine against CSFV infections.

Animals↗

PubMed2006

[Congenital hyperinsulinism: a difficult and complicated case study].

This paper reported a case of congenital hyperinsulinism and reviewed the relevant literatures regarding to the etiology, pathogenesis, clinical and pathological features, diagnosis and treatment of this disorder. The baby (male), with gestational age of 36 weeks and birth weight 4,200 g, was delivered by caesarean section. It presented with hypoglycemia immediately after birth (0.8 mmol/L). Through the course of the disease, the baby's blood sugar manifested with 1.2-2.8 mmol/L although glucocorticoid was administered. 10% glucose solutions were intravenously infused at a speed of 10-17 mg/(kg x min) for this patient to retain a stable blood sugar level. The plasma insulin level was 24.13 U/L and blood sugar level was 1.5 mmol/L on day 30 of his life. The ratio of plasma insulin (U/L) and plasma glucose (mg/dL) was 0.89. These results suggest an inappropriate insulin secretion resulting in persistent hypoglycemia in this baby and so it was definitely diagnosed with congenital hyperinsulinism.

Blood Glucose↗

PubMed2005

[Endothelial cells and cardiac explants in three-dimensional culture system].

To observe the morphological features of endothelial cells and cardiac explants cultured in two- or three-dimensional culture systems, several three-dimensional collagen type I culture systems, such as the in gel, on gel, sandwich model, and the microscope slide model, were used to examine the growth patterns of the cells and explants from heart by using immunofluorescence staining and microscopic observation in the presence or absence of vascular endothelial growth factor (VEGF). In two-dimensional cultures the primary cardiac endothelial cells arrayed into a cobblestone-like structure. When cultured in three-dimensional matrix, the cells were elongated and migrated into the gel, with a phenotype similar to that in the process of angiogenesis and vasculogenesis in vivo. VEGF promoted the process of the endothelial cells transforming into tube-like structure. Cardiac explants grew well in the collagen gel. Adjacent explants were connected to each other by the migrating cells with the occurrence of autorhythmic beating of the explants. Thin-layer collagen gel, microscope slide chamber and aorta-strip model were also tested and proved to be good tools for vasculogenesis or angiogenesis studies. Three-dimensional culture systems enable the endothelial cells to proliferate, migrate, and anchor to three-dimensional vascular structures, showing advantages for observing the feature of angiogenesis. Different three-dimensional culture models may be used for variable research purposes.

Animals↗

PubMed2005

[Mechanisms of sensitization by 8-chloro-adenosine of human tumor cells to TRAIL-induced apoptosis].

OBJECTIVE: To study the effect of 8-chloro-adenosine (8-Cl-Ado) on the sensitivity of human hepatoma and breast cancer cell lines to TRAIL-induced apoptosis in vitro and its mechanisms. METHODS: Recombinant soluble TRAIL (rsTRAIL) or 8-Cl-Ado was used to treat hepatoma cell line BEL-7402 and breast cancer cell line MCF-7 in vitro. MTT assay was used to evaluate cell viability. The effect of cotreatment with rsTRAIL and 8-Cl-Ado was analyzed. NF-kappaB activity reporter plasmid was designed to measure the activity of transcription factor NF-kappaB. After transient transfection with the reporter plasmid, which contains NF-kappaB-responsive elements, into the cell lines, cells were treated with rsTRAIL and/or 8-Cl-Ado, then the activity of the reporter gene luciferase was determined. Different kinds of caspase inhibitors were used to measure the effect of caspases in the rsTRAIL and/or 8-Cl-Ado induced apoptosis. RESULTS: 8-Cl-Ado could greatly enhance sensitivity of BEL-7402 and MCF-7 cells to reTRAIL. Treatment with 8-Cl-Ado and rsTRAIL inactivated transcription factor NF-kappaB and induced apoptosis in BEL-7402, but not in MCF-7. Caspase family inhibitor could not prevent apoptosis induced by 8-Cl-Ado and rsTRAIL in BEL-7402 cells, however, it could block apoptosis in MCF-7 cells, indicating that two different apoptosis pathways in MCF-7 and BEL-7402 might exist, one was caspase dependent and the other caspase independent. Moreover, all of the inhibitors of caspse-3, -8 and -9 could not block apoptosis induced by the co-treatment. CONCLUSION: 8-chloro-adenosine can enhance the sensitivity of human hepatoma cell line BEL-7402 and breast cancer cell line MCF-7 to rsTRAIL, even though MCF-7 is TRAIL-resistant. 8-Cl-Ado combined with rsTRAIL can trigger different signal pathways in MCF-7 and BEL-7402, which are caspase dependent and independent, respectively.

2-Chloroadenosine↗

PubMed2004

Cellular distribution of GPR14 and the positive inotropic role of urotensin II in the myocardium in adult rat.

Urotensin II is a cyclic neuropeptide recently shown to play a role via its receptor GPR14 in regulating vascular tone in the mammalian cardiovascular system. The existence of GPR14 in rat heart has been validated by ligand binding assay and RT-PCR. In the present study, we investigated the cellular distribution of GPR14 protein in rat heart by using immunohistochemistry and confocal microscopic immunofluorescence double staining with antipeptide polyclonal antibodies against GPR14 and cell type markers for myocytes and endothelial cells. The direct effect of urotensin II on left ventricular contractility was further evaluated in isolated left ventricular papillary muscles of the rat. In paraffin-embedded heart sections, positive immunohistochemical staining was observed in the left ventricle but not in the right ventricle and atria. Immunofluorescence double staining revealed the cardiac myocyte as the only cell type expressing GPR14 protein in frozen heart sections as well as in isolated cardiac myocytes. There was no visible signal for GPR14 in intramyocardial coronary arteries and capillaries. The existence of GPR14 protein in rat heart was further validated by immunoprecipitation and Western blot analysis. In isolated rat left ventricular papillary muscle preparations, urotensin II induced an increase in active contractile force. GPR14 mRNA was also detected in rat heart by RT-PCR. These data provide the first direct evidence for the cellular localization of GPR14 receptor protein and a positive inotropic effect of urotensin II in normal rat heart.

Age Factors↗

PubMed2003

Role of angiotensin AT1 and AT2 receptors in cardiac hypertrophy and cardiac remodelling.

1. Left ventricular hypertrophy (LVH) is an independent cardiovascular risk factor. Angiotensin AT1 receptor antagonism has been considered as a specific approach to block the renin-angiotensin system and been demonstrated to be able to prevent or regress LVH by interfering with the remodelling process of the heart. 2. Angiotensin AT1 receptor blockade induces a marked increase in angiotensin (Ang) II, which may stimulate the AT2 receptors. Gene expression of AT1 and AT2 receptors increases in a time-dependent manner in cardiac remodelling following myocardial infarction. 3. Considerable efforts have been made to clarify the role of AT2 receptors in cardiac hypertrophy and remodelling since the mid-1990s, resulting in controversial reports: the AT2 receptor mediates actions either opposite to or in coordination with those of the AT1 receptor. Moreover, there are many reports of no significant effects mediated by AT2 receptors. 4. Based on the studies reviewed in the present article, we assume that the predominant effect of AngII in cardiac hypertrophy and cardiac remodelling is growth promoting and that this effect is mediated mainly via AT1 receptors. The AT2 receptors may affect the hypertrophic process by interacting with other cardiac membrane proteins, enzymes and autacoids. Before coming to a conclusion as to whether AT2 receptor stimulation or antagonism is beneficial to the heart, more studies should be performed in different LVH models, especially long-term treatment protocols in vivo.

Angiotensin II↗