Xuping Qin

University of South China, Heng-nan, Hunan, China

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Publications (4)8.71 Total impact

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    ABSTRACT: The aim of this study was to investigate the role of apelin in the cell proliferation and autophagy of lung adenocarcinoma. The over-expression of APJ in lung adenocarcinoma was detected by immunohistochemistry, while plasma apelin level in lung cancer patients was measured by enzyme-linked immunosorbent assay. Our findings revealed that apelin-13 significantly increased the phosphorylation of ERK1/2, the expression of cyclin D1, microtubule-associated protein 1 light chain 3A/B (LC3A/B), and beclin1, and confirmed that apelin-13 promoted A549 cell proliferation and induced A549 cell autophagy via ERK1/2 signaling. Moreover, there are pores on the surface of human lung adenocarcinoma cell line A549 and apelin-13 causes cell surface smooth and glossy as observed under atomic force microscopy. These results suggested that ERK1/2 signaling pathway mediates apelin-13-induced lung adenocarcinoma cell proliferation and autophagy. Under our experimental condition, autophagy associated with 3-methyladenine was not involved in cell proliferation.
    Acta Biochimica et Biophysica Sinica 12/2013; · 1.81 Impact Factor
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    ABSTRACT: Vascular smooth muscle cells (VSMCs) were prepared from thoracic aortas of male Sprague-Dawley rats by the explant method to observe VSMC proliferation via phosphoinositide 3 kinase (PI3K)/Akt signaling transduction pathway induced by apelin-13. Expression of PI3K, phospho-PI3K, phospho-Akt, ERK1/2, phospho-ERK1/2 and cyclin D1 was detected by western blot analysis. Results showed that apelin-13 promoted the expression of phospho-PI3K and phospho-Akt in dose- and timedependent manner. PI3K inhibitor LY294002 significantly decreased the expression of phospho-PI3K, phospho-Akt, phospho-ERK1/2, and cyclin D1 induced by apelin-13. The Akt inhibitor 1701-1 significantly diminished the expression of phospho-Akt, phospho-ERK1/2, and cyclin D1 stimulated by apelin-13. MTT assay results showed that PI3K inhibitor LY294002 and Akt inhibitor 1701-1 significantly inhibited the VSMC proliferation induced by apelin-13. Apelin-13 promoted VSMC proliferation through PI3K/Akt signaling transduction pathway.
    Acta Biochimica et Biophysica Sinica 06/2010; 42(6):396-402. · 1.81 Impact Factor
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    ABSTRACT: To investigate whether apelin-13 induced THP-1 monocytes (MCs) adhesion to ECV304 human umbilical vein endothelial cells (HUVECs) via 14-3-3 signaling transduction pathway and the potential novel physiological function and signaling transduction pathway of apelin-APJ, HUVECs ECV304 were cultured in DMEM and MCs THP-1 were cultured in RPMI 1640 medium. Monocyte adhesion and the expression of vascular cell adhesion molecule-1 (VCAM-1) and 14-3-3 were measured with monocyte adhesion assay and western blot analysis. Data showed that apelin-13 increased adhesion of MCs to HUVECs in a concentration- and time-dependent manner, which reached their peaks at 1 mM and 12 h, respectively. Similarly, apelin-13 induced the expression of HUVECs adhesion molecule, VCAM-1, in a concentration- and time-dependent manner, reached their peaks at 1 microM and 12 h, respectively. Apelin-13 induced the expression of 14-3-3 in a concentration- and timedependent manner, which reached their peaks at 1 mM and 5 min, respectively. Furthermore, the potent 14-3-3 inhibitor difopein significantly reduced the expression of 14-3-3 and VCAM-1 in apelin-13 stimulated HUVECs, and difopein significantly inhibited the effect of apelin-13 on induction of MCs adhesion to HUVECs. These data suggested that 14-3-3 mediated the induction of adhesion of MCs to HUVECs by Apelin-13.
    Acta Biochimica et Biophysica Sinica 06/2010; 42(6):403-9. · 1.81 Impact Factor
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    ABSTRACT: Apelin is the endogenous ligand of the G protein-coupled receptor, APJ. Vascular smooth muscle cells express both apelin and APJ, which are important regulatory factors in the cardiovascular and nervous systems. Importantly, APJ is also involved in the pathogenesis if HIV-1 infection. We investigated whether vascular smooth muscle cell proliferation was regulated through an apelin-pERK1/2-cyclin D1 signal transduction pathway. Apelin-13 significantly stimulated vascular smooth muscle cell proliferation and increased cell cycle progression. Apelin-13 a decreased the proportion of cell in the G0/G1 phase while increasing the number of cells in S phase. Apelin-13 also increased the levels of cyclin D1, cyclin E and pERK1/2. Treatment of cells with the MEK inhibitor PD98059 attenuated the apelin-3-induced pERK1/2 activation. Similarly, treatment with PD98059 partially diminished the apelin-13-induced expression of cyclin D1 and vascular smooth muscle cell proliferation. Taken together, these data established that apelin-13 stimulates vascular smooth muscle cell proliferation by promoting the G1-S phase transition, and that this effect is mediated in part by an apelin-pERK1/2-cyclin D1 signal cascade.
    Frontiers in Bioscience 02/2008; 13:3786-92. · 3.29 Impact Factor

Publication Stats

28 Citations
8.71 Total Impact Points


  • 2010
    • University of South China
      Heng-nan, Hunan, China
  • 2008
    • Nanhua University