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김훈,이중섭,곽성욱,정지은,김태경,Chenxiong Xu,홍종산,Zhehu Li,김선명,황광연,홍기창,유승권,최윤재,김형기 한국분자세포생물학회 2006 Molecules and cells Vol.21 No.2
We have established in culture a spontaneously immortalized bovine embryonic fibroblast (BEF) cell line that has lost p53 and p16INK4a functions. MyoD is a musclespecific regulator capable of inducing myogenesis in a number of cell types. When the BEF cells were transduced with MyoD they differentiated efficiently to desmin- positive myofibers in the presence of 2% horse serum and 1.7 nM insulin. The myogenic differentiation of this cell line was more rapid and obvious than that of C2C12 cells, as judged by morphological changes and expression of various muscle regulatory factors. To confirm that lack of the p53 and p16INK4a pathway does not prevent MyoD-mediated myogenesis, we established a cell line transformed with SV40LT (BEFV) and introduced MyoD into it. In the presence of 2% horse serum and 1.7 nM insulin, the MyoD-transduced BEFV cells differentiated like the MyoD-transduced BEFS cells, and displayed a similar pattern of expression of muscle regulatory proteins. Taken together, our results indicate that MyoD overexpression overcomes the defect in muscle differentiation associated with immortalization and cell transformation caused by the loss of p53 and Rb functions.
Establishment and Characterization of Three Immortal Bovine Muscular Epithelial Cell Lines
진선,이중섭,곽성욱,이수연,정지은,김태경,Chenxiong Xu,홍종산,Zhehu Li,김선명,Xumin Pian,이동희,윤종택,유승권,최윤재,김형기 한국분자세포생물학회 2006 Molecules and cells Vol.21 No.1
We have established three immortal bovine muscularepithelial (BME) cell lines, one spontaneously immortalized(BMES), the second SV40LT-mediated (BMEV)and the third hTERT-mediated (BMET). The morphologyof the three immortal cell lines was similar tothat of early passage primary BME cells. Each of theimmortal cell lines made cytokeratin, a typical epithelialmarker. BMET grew faster than the other immortallines and the BME cells, in 10% FBS-DMEM medium,whereas neither the primary cells nor the threeimmortal cell lines grew in 0.5% FBS-DMEM. Theprimary BME cells and the immortal cell lines, withthe exception of BMES, made increasing amounts ofp53 protein when treated with doxorubicin, a DNAdamaging agent. On the other hand, almost half of thecells in populations of the three immortal cell linesmay lack p16INK4a regulatory function, compared toprimary BME cells that were growth arrested by enforcedexpression of p16INK4a. In soft-agar assays, theprimary cells and immortal cell lines proved to be lesstransformed in phenotype than HeLa cells. The threeimmortal epithelial-type cell lines reported here arethe first cell lines established from muscle tissue ofbovine or other species.
Jin, Xun,Lee, Joong-Seub,Kwak, Sungwook,Jung, Ji-Eun,Kim, Tae-Kyung,Xu, Chenxiong,Hong, Zhongshan,Li, Zhehu,Kim, Sun-Myoung,Whang, Kwang Youn,Hong, Ki-Chang,You, Seungkwon,Choi, Yun-Jaie,Kim, Hyunggee Korean Society for Molecular Biology 2006 Molecules and cells Vol.21 No.2
<P>We have established in culture a spontaneously immortalized bovine embryonic fibroblast (BEF) cell line that has lost p53 and p16(INK4a) functions. MyoD is a muscle-specific regulator capable of inducing myogenesis in a number of cell types. When the BEF cells were transduced with MyoD they differentiated efficiently to desmin-positive myofibers in the presence of 2% horse serum and 1.7 nM insulin. The myogenic differentiation of this cell line was more rapid and obvious than that of C2C12 cells, as judged by morphological changes and expression of various muscle regulatory factors. To confirm that lack of the p53 and p16(INK4a) pathway does not prevent MyoD-mediated myogenesis, we established a cell line transformed with SV40LT (BEFV) and introduced MyoD into it. In the presence of 2% horse serum and 1.7 nM insulin, the MyoD-transduced BEFV cells differentiated like the MyoD-transduced BEFS cells, and displayed a similar pattern of expression of muscle regulatory proteins. Taken together, our results indicate that MyoD overexpression overcomes the defect in muscle differentiation associated with immortalization and cell transformation caused by the loss of p53 and Rb functions.</P>