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Mao X.-H.,University of South China | Mao X.-H.,Hunan Environment Biological Polytechnic College | Su T.,University of South China | Zhang X.-H.,University of South China | And 5 more authors.
Progress in Biochemistry and Biophysics | Year: 2011

Previously we reported that G protein-coupled receptor APJ endogenous ligand apelin-13 induced adhesion of monocytes to human umbilical vein endothelial cells (HUVECs).Now we investigated whether phosphatidylinositol 3-kinase (PI3K) signaling pathway mediated monocytes (MCs) adhesion to HUVECs induced by apelin-13. Human umbilical vein endothelial cell line ECV304 was cultured in DMEM medium and the monocyte cell line THP-1 was cultured in 1640 medium. Myeloperoxidase(MPO) assay was used to identify effects of monocytes adhesion to HUVECs. Expression of vascular cell adhesion molecule (VCAM)-1, phospho-PI3K and PI3K were detected by Western blotting. Apelin-13 promoted PI3K phosphorylation in concentration-dependent and time-dependent manner, which reached the peak at 1 μmol/L and 30 min respectively. The PI3K inhibitor LY294002 inhibited PI3K phosphorylation and the expression of VCAM-1 in HUVECs induced by apelin-13. And the PI3K inhibitor LY294002 inhibited the MCs adhesion to HUVECs induced by apelin-13. It can be concluded that apelin-13 promoted monocytes adhesion to HUVECs through VCAM-1 mediated by PI3K signaling pathway.

Pan W.-N.,University of South China | Pan W.-N.,Hunan Food and Drug Voctional College | Li F.,University of South China | Mao X.-H.,University of South China | And 8 more authors.
Progress in Biochemistry and Biophysics | Year: 2011

Previously, we found that G protein-coupled receptor APJ endogenous ligand apelin-13 stimulates vascular smooth muscle cells (VSMC) proliferation mediated in part by PKC-PI3K-ERK1/2-cyclinD1 signaling cascades. In this study, Raf-1-14-3-3 signaling in rat VSMCs proliferation stimulated by apelin-13 was further investigated. Cell proliferation was measured with MTT assay. Expression of PI3K, phospho-PI3K, Raf-1, phospho-Raf-1, ERK1/2, phospho-ERK1/2, cyclinD1 and cyclinE were detected by Western blotting. 14-3-3 protein combining with Raf-1 was detected by immunoprecipitation. Here, we demonstrated that apelin-13 increased the expression of 14-3-3, Raf-1 phosphorylation and ERK1/2 phosphorylation in a concentration-dependent and time-dependent manner at 0 ∼ 4 μmol/L and 0 ∼ 48 h. 14-3-3 inhibitor Difopein decreased the apelin-13-induced Raf-1 phosphorylation, ERK1/2 phosphorylation, expression of cyclinD1 and cyclinE. Furthermore, apelin-13 promoted the combination of 14-3-3 protein and Raf-1, Difopein significantly inhibited the combination of 14-3-3 and Raf-1 stimulated by apelin-13. Similarly, Difopein significantly inhibited the VSMCs proliferation stimulated by apelin-13. Our results revealed that Raf-1 +14-3-3-ERK1/2 signaling cascades mediated the effect of apelin-13 on rat VSMCs proliferation.

Dai W.,Chinese Academy of Sciences | Dai W.,Hunan Environment Biological Polytechnic College | He W.,Chinese Academy of Sciences | Shang G.,Nanjing Normal University | And 3 more authors.
American Journal of Physiology - Heart and Circulatory Physiology | Year: 2010

Our previous studies proved that myofibrillogenesis regulator (MR)-1 has a close relationship with cardiac hypertrophy induced by ANG II. In the present study, we developed a recombinant adenoviral vector (AdSiRMR-1) driving small interfering (si)RNA against MR-1 to evaluate its effect on cardiac hypertrophy in vivo. Cardiac hypertrophy was induced by chronic ANG II infusion in mice; AdSiR-MR-1 was administered via the jugular vein through one bolus injection. Thirteen days after the injection, viral DNA was still detectable in the heart, validating the efficiency of gene transfer. Expression levels of MR-1 mRNA and protein were increased by 2.5-fold in the heart after ANG II infusion; AdSiR-control, which contained a scrambled siRNA sequence, had no effect on them. AdSiR-MR-1 treatment abolished the upregulation of MR-1 induced by ANG II. The silencing effect of AdSiR-MR-1 was observed in many other tissues, such as the liver, lung, and kidney, except skeletal muscle. ANG II-induced cardiac hypertrophy was suppressed in mice treated with AdSiR-MR-1, as determined by echocardiography. Morphological and immnohistochemical examinations revealed that interstitial cardiac fibrosis as well as infiltrating inflammatory cells were increased after ANG II infusion; AdSiR-MR-1 greatly ameliorated these disorders. In ANG II-infused mice, MR-1 silencing also blocked the upregulation of other genes related to cardiac hypertrophy or metabolism of the extracellular matrix. In summary, our results demonstrate the feasibility of MR-1 silencing in vivo and suggest that MR-1 could be a potential new target to treat cardiac hypertrophy induced by ANG II. Copyright © 2010 the American Physiological Society.

Qiu Q.-C.,University of South China | Qiu Q.-C.,Vanderbilt University | Hu B.,University of South China | Hu B.,Vanderbilt University | And 7 more authors.
Genetics and Molecular Biology | Year: 2012

STGC3 is a potential tumor suppressor that inhibits the growth of the nasopharyngeal carcinoma cell line CNE2; the expression of this protein is reduced in nasopharyngeal carcinoma compared with normal nasopharyngeal tissue. In this study, we investigated the tumor-suppressing activity of STGC3 in nude mice injected subcutaneously with Tet/pTRE-STGC3/CNE2 cells. STGC3 expression was induced by the intraperitoneal injection of doxycycline (Dox). The volume mean of Tet/pTRE-STGC3/CNE2+Dox xenografts was smaller than that of Tet/pTRE/CNE2+Dox xenografts. In addition, Tet/pTRE-STGC3/CNE2+Dox xenografts showed an increase in the percentage of apoptotic cells, a decrease in Bcl-2 protein expression and an increase in Bax protein expression. A proteomic approach was used to assess the protein expression profile associated with STGC3-mediated apoptosis. Western blotting confirmed the differential up-regulation of prohibitin seen in proteomic analysis. These results indicate that overexpression of STGC3 inhibits xenograft growth in nude mice by enhancing apoptotic cell death through altered expression of apoptosis-related proteins such as Bcl-2, Bax and prohibitin. These data contribute to our understanding of the function of STGC3 in human nasopharyngeal carcinoma and provide new clues for investigating other STGC3-associated tumors. © 2012, Sociedade Brasileira de Genética.

Dai W.,Chinese Academy of Sciences | Dai W.,Hunan Environment Biological Polytechnic College | chen H.,Hunan Environment Biological Polytechnic College | Jiang J.,Chinese Academy of Sciences | And 2 more authors.
Biochemical and Biophysical Research Communications | Year: 2010

Myofibrillogenesis regulator-1(MR-1) can aggravate cardiac hypertrophy induced by angiotensin(Ang) II in mice through activation of NF-κB signaling pathway, and nuclear transcription factor (NF)-κB and activator protein-1(AP-1) regulate inflammatory and immune responses by increasing the expression of specific inflammatory genes in various tissues including heart. Whether inhibition of MR-1 expression will attenuate AngII-induced inflammatory injury in mice heart has not been explored. Herein, we monitored the activation of NF-κB and AP-1, together with expression of pro-inflammatory of interleukin(IL)-6, tumor necrosis factor(TNF)-α, vascular-cell adhesion molecule (VCAM)-1, platelet endothelial cell adhesion molecule (PECAM), and inflammatory cell infiltration in heart of mice which are induced firstly by AngII (PBS),then received MR-1-siRNA or control-siRNA injecting. We found that the activation of NF-κB and AP-1 was inhibited significantly, together with the decreased expression of IL-6, TNF-α, VCAM-1, and PECAM in AngII-induced mice myocardium in MR-1-siRNA injection groups compared with control-siRNA injecting groups. However, the expression level of MR-1 was not an apparent change in PBS-infused groups than in unoperation groups, and MR-1-siRNA do not affect the expression of MR-1 in PBS-infused mice. Our findings suggest that silencing MR-1 protected mice myocardium against inflammatory injury induced by AngII by suppression of pro-inflammatory transcription factors NF-κB and AP-1 signaling pathway. © 2009 Elsevier Inc. All rights reserved.

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