|本期目录/Table of Contents|

[1]杨俊英,李晓霞.BICC1对骨髓基质细胞定向分化的调控作用研究[J].天津医科大学学报,2020,26(03):199-203.
 YANG Jun-ying,LI Xiao-xia.The role of BICC1 in osteogenic and adipogenic differentiation of bone marrow stromal cells[J].Journal of Tianjin Medical University,2020,26(03):199-203.
点击复制

BICC1对骨髓基质细胞定向分化的调控作用研究(PDF)
分享到:

《天津医科大学学报》[ISSN:1006-8147/CN:12-1259/R]

卷:
26卷
期数:
2020年03期
页码:
199-203
栏目:
基础医学
出版日期:
2020-06-10

文章信息/Info

Title:
The role of BICC1 in osteogenic and adipogenic differentiation of bone marrow stromal cells
文章编号:
1006-8147(2020)03-0199-05
作者:
杨俊英李晓霞
(天津医科大学基础医学院病原生物学系,天津300070)
Author(s):
YANG Jun-ying LI Xiao-xia
(Department of Pathogen Biology,School of Basic Medical Sciences, Tianjin Medical University, Tianjin 300070, China)
关键词:
Bicc1骨髓基质细胞分化成骨细胞脂肪细胞
Keywords:
Bicc1bone marrow stromal cellsdifferentiationosteoblast adipocyte
分类号:
R37
DOI:
-
文献标志码:
A
摘要:
目的:探讨BICC1在骨髓基质细胞向成骨细胞及脂肪细胞分化过程中的作用。方法:构建Bicc1过表达质粒Bicc1-pcDNA3.1,以pcDNA3.1为对照,分别转染小鼠骨髓基质细胞ST2。对两组细胞进行成脂和成骨诱导,在成骨诱导14 d时碱性磷酸酶染色检测成骨分化情况,在成脂诱导5 d时利用油红O染色检测脂滴形成情况;采用qRT-PCR及Western blot技术检测细胞Bicc1过表达对成骨及成脂相关因子的影响。结果:酶切及测序结果显示Bicc1过表达质粒构建成功,将其转染到ST2细胞后,Bicc1 mRNA表达水平较对照组升高15.23倍(P<0.05)。成骨诱导条件下,Bicc1过表达组ST2细胞碱性磷酸酶染色增强,成骨相关因子Osterix、碱性磷酸酶、Osteopontin、Runt相关转录因子2(Runx2)和骨钙素的mRNA和/或蛋白表达水平显著上升(均P<0.05)。成脂诱导条件下, Bicc1过表达组ST2细胞中脂滴形成减少,油红OD520较对照组明显降低(P<0.01),成脂相关因子过氧化物酶体增殖物活化受体γ(PPARγ)、CCAAT增强子结合蛋白α(C/EBPα)、脂肪酸结合蛋白(FABP4/aP2)和adipsin的mRNA及蛋白表达水平显著下降(均P<0.05)。结论:BICC1可促进骨髓基质细胞向成骨细胞分化,抑制其向脂肪细胞分化。
Abstract:
Objective: To study the role of BICC1 in osteogenic and adipogenic differentiation of bone marrow stromal cells. Methods:Bicc1 expression construct was made and transfected into mouse marrow stromal cell line ST2. The cells transfected with the vector pcDNA3.1 served as control. The transfected cells were subjected to osteogenic treatment for 14 days or adipogenic treatment for 5 days. For the osteogenic differentiation assay, alkaline phosphatase(ALP) staining was done and the expression of osteogenic factors were examined by using qRT-PCR and Western blot. For the adipogenic differentiation assay, oil-red O staining was done and the expression of adipogenic factors were examined. Results:The identify of the Bicc1 overexpression plasmid was verified by enzyme digestion and DNA sequencing. The Bicc1 mRNA in over-expressed group was markedly increased compared with control group (15.23-fold difference, P<0.05). Following osteogenic induction, Bicc1 overexpression stimulated the differentiation of osteoblasts from ST2 cells as compared to vector transfection, as evidenced by the enhanced ALP staining and the increased mRNA and protein levels of osteogenic factors such as osterix, ALP, osteopontin, Runt-related transcription factor (Runx2) and osteocalcin(all P<0.05). Following adipogenic induction, Bicc1 overexpression inhibited the differentiation of adipocytes from ST2 cells, as evidenced by the attenuated oil-red O staining and the decreased mRNA and protein levels of adipogenic factors such as peroxisome proliferator-activated receptor γ(PPARγ), CCAAT enhancer-binding protein α (C/EBPα), fatty acid-binding protein 4(FABP4/aP2) and adipsin(all P<0.05). Conclusion:BICC1 promotes osteogenic differentiation and suppresses adipogenic differentiation of bone marrow stromal cells.

参考文献/References:

[1] Tontonoz P, Spiegelman B M. Fat and beyond: the diverse biology of PPARgamma[J]. Annu Rev Biochem, 2008, 77: 289
[2] Hong J W, Park K W. Further understanding of fat biology: lessons from a fat fly[J]. Exp Mol Med, 2010, 42(1):12
[3] Gimble J M, Nuttall M E. The relationship between adipose tissue and bone metabolism[J]. Clin Biochem, 2012, 45(12):874
[4] Ambrosi Th H, Scialdone A, Graja A, et al. Adipocyte accumulation in the bone marrow during obesity and aging impairs stem cell-based hematopoietic and bone regeneration[J]. Cell Stem Cell,2017, 20(6):771
[5] Berendsen A D, Olsen B R. Osteoblast-adipocyte lineage plasticity in tissue development, maintenance and pathology[J]. Cell Mol Life Sci, 2014, 71(3):493
[6] Dowdle M E, Park S, Imboden S B, et al. A single KH domain in Bicaudal-C links mRNA binding and translational repression functions to maternal development[J]. Development, 2019, 146(10):1477
[7] Dai X X, Jiang J C, Sha Q Q, et al. A combinatorial code for mRNA 3′-UTR-mediated translational control in the mouse oocyte[J]. Nucleic Acids Res, 2019, 47(1):328
[8] Bouvrette D J, Price S J, Bryda E C. K homology domains of the mouse polycystic kidney disease-related protein,Bicaudal-C(Bicc1),mediate RNA binding in vitro[J]. Nephron Exp Nephrol, 2008, 108(1):e27
[9] Piazzon N, Bernet F, Guihard L, et al. Urine Fetuin-A is a biomarker of autosomal dominant polycystic kidney disease progression[J]. J Transl Med, 2015, 13:103
[10] Leal-Esteban L C, Rothé B, Fortier S, et al. Role of bicaudal C1 in renal gluconeogenesis and its novel interaction with the CTLH complex[J]. PLoS Genet, 2018, 14(7):e1007487
[11] Mashima T, Seimiya H, Tsuruo T. De novo fatty-acid synthesis and related pathways as molecular targets for cancer therapy[J]. Br J Cancer, 2009, 100(9):1369
[12] Foo J N, Xia Y. Polycystic kidney disease: new knowledge and future promises[J]. Curr Opin Genet Dev, 2019, 56:69
[13] Xiao Z S, Cao L, Liang Y J, et al. Osteoblast-specific deletion of Pkd2 leads to low-turnover osteopenia and reduced bone marrow adiposity[J]. PLoS One, 2014,9(12):e114198
[14] Xiao Z S, Baudry J, Cao L, et al. Polycystin-1 interacts with TAZ to stimulate osteoblastogenesis and inhibit adipogensis[J]. J Clin Invest, 2018, 128(1):157
[15] Lian P W, Li A, Li Y, et al. Loss of polycystin-1 inhibits Bicc1 expression during Mouse Development[J]. PLoS One, 2014, 9(3):e88816
[16] Gamberi C, Lasko P. The Bic-C family of developmental translational regulators[J]. Comp Funct Genomics, 2012,2012:141386
[17] Gamberi C, Hipfner D R, Trudel M, et al. Bicaudal C mutation causes myc and TOR pathway up-regulation and polycystic kidney disease-like phenotypes in Drosophila[J]. PLoS Genet, 2017,13(4): e1006694
[18] Mesner L D, Ray B, Hsu Y H, et al.Bicc1 is a genetic determinant of osteoblastogenesis and bone mineral density[J]. J Clin Invest, 2014, 124(6):2736
[19] Chen X, Wang Z Q, Duan N, et al. Osteoblast-osteoclast interactions[J]. Connect Tissue Res, 2018, 59(2):99
[20] Chen R J, Qiu H M, Tong Y, et al. MiRNA-19a-3p alleviates the progression of osteoporosis by targeting HDAC4 to promote the osteogenic differentiation of hMSCs[J]. Biochem Biophys Res Commun, 2019, 516(3):666
[21] Guan X, Gao Y, Zhou J, et al. miR-223 regulates adipogenic and osteogenic differentiation of mesenchymal stem cells through a C/EBPs/miR-223/FGFR2 regulatory feedback loop[J]. Stem Cells, 2015, 33(5):1589
[22] Yu W H, Li F G, Chen X Y, et al. PPARγ suppression inhibits adipogenesis but does not promote osteogenesis of human mesenchymal stem cells[J]. Int J Biochem Cell Biol, 2012, 44(2):377
[23] Han Y, Kim C Y, Cheong H, et al. Osterix represses adipogenesis by negatively regulating PPAR gamma transcriptional activity[J]. Sci Rep, 2016, 6:35655

相似文献/References:

备注/Memo

备注/Memo:
基金项目 国家自然科学基金资助项目(81772297)
作者简介 杨俊英(1994-),女,硕士在读,研究方向:病原生物学;通信作者:李晓霞,E-mail: lilian_lxx@126.com。
更新日期/Last Update: 2020-06-13