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- 저자 : Quan Chengshi (검색결과 2 건)
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Zhang, Mingzi,Ahn, Woosung,Kim, Sumin,Hong, Hyun Sook,Quan, Chengshi,Son, Youngsook John Wiley & Sons Ltd. 2017 Microcirculation Vol.24 No.8
<P><B>Abstract</B></P><P><B>Objective</B></P><P>The aim of this study was to evaluate the angiogenicity of a combination of BM‐EPCs and BM‐MSCs in vitro in the presence of SP and its working mechanism.</P><P><B>Methods</B></P><P>BM‐MSCs and BM‐EPCs were cocultured with or without SP. ELISA and RT‐PCR were performed to detect angiogenic factors such as VEGF and PDGF‐BB. N‐cadherin was detected by Western blot analysis. The tubular network‐forming ability was evaluated by a Matrigel tube‐forming assay.</P><P><B>Results</B></P><P>BM‐EPCs coculture with BM‐MSCs strongly stimulated the recruitment of BM‐MSCs onto the BM‐EPC‐generated endothelial tubular network. Upon SP treatment, endothelial branching point, tubule length, and tubular recruitment of BM‐MSCs were further increased and stabilized. The coculture of BM‐EPCs and BM‐MSCs synergistically stimulated expression of VEGF, VEGF receptor, N‐cadherin, and PDGF‐BB, all of which were further enhanced by SP treatment. Blockade of PDGF‐BB by its functional blocking antibodies markedly reduced the BM‐MSC incorporation into the endothelial tubules. SP‐pretreated BM‐MSCs were preferentially incorporated into the preformed BM‐EPC tubular network.</P><P><B>Conclusions</B></P><P>BM‐EPCs along with SP promote the pericyte‐like coverage of BM‐MSCs on endothelial tubules possibly through the induction of PDGF‐BB.</P>
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Role of Estrogen Receptor-α in the Regulation of Claudin-6 Expression in Breast Cancer Cells
Liu Yafang,Wu Qiong,Ren Yue,Xu Xiaoming,Yu Lina,Zhang Mingzi,Zhang Ting,Li Yulin,Quan Chengshi 한국유방암학회 2011 Journal of breast cancer Vol.14 No.1
Purpose: In our previous studies we showed that upregulating claudin-6 (CLDN6) expression may contribute to preventing breast cancer, and that 17β-estradiol induces a concentration- and time-related effect on CLDN6 mRNA and protein expression in MCF-7 cells. However, the mechanisms of 17β-estradiol regulation of CLDN6 are still unclear. We determined the role of estrogen receptors in the regulation of CLDN6 expression in human breast cancer tissues and a cell line. Methods: CLDN6, estrogen receptor alpha (ERα) and estrogen receptor beta (ERβ) expression in breast cancer tissues were examined using immunohistochemistry. The human breast cancer cell line, MCF-7, which expresses ERα but not ERβ was used. CLDN6 and ERα expression were measured by reverse transcriptase-PCR, Western blotting and immunofluorescent staining. Treatments with propyl pyrazole triol (PPT) and ICI 182, 780 (ICI) were performed. Results: The results revealed that CLDN6 expression was related to ERα in breast cancer tissues (p=0.033). PPT, an ERα-selective ligand, upregulated CLDN6 expression at 10^(-5) mol/L after 24 hours. The effect of PPT on regulating CLDN6 expression in MCF-7 cells was blocked by ICI. Conclusion: These findings suggest that Erα reulates CLDN6 expression in breast cancer tissues and that 17β- estradiol induces CLDN6 expression through an ERα pathway in MCF-7 cells.
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