Down-regulated miR-15a mediates the epithelial-mesenchymal transition in renal tubular epithelial cells promoted by high glucose

被引：7
作者：
Sun, Tingli [1 ]
Yang, Jun [1 ]
Dong, Wenpeng [1 ]
Wang, Ruiyan [1 ]
Ma, Peilong [1 ]
Kang, Ping [1 ]
Zhang, Hongbo [1 ]
Xie, Changying [1 ]
Du, Juan [1 ]
Zhao, Lijie [2 ]
机构：
[1] Gen Hosp Daqing Oil Field, Dept Nephrol, Daqing, Peoples R China
[2] Gen Hosp Daqing Oil Field, Dept Geriatr, Daqing, Peoples R China
来源：
BIOSCIENCE BIOTECHNOLOGY AND BIOCHEMISTRY | 2014年 / 78卷 / 08期
关键词：
high glucose; miR-15a; epithelial-mesenchymal transition (EMT); renal tubular epithelial cells; AP4; NEGATIVE FEEDBACK LOOP; GROWTH-FACTOR-BETA; DIABETIC-NEPHROPATHY; COLORECTAL-CANCER; METASTASIS; MICRORNA; GENE; EXPRESSION; FIBROSIS; DISEASE;
D O I：
10.1080/09168451.2014.936345
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
High glucose (HG) has been reported to be associated with renal dysfunction. And one potential mechanism underlining the dysfunction is the epithelial-mesenchymal transition (EMT) of renal tubular epithelial cells. Present study showed that EMT was induced in the HG-treated renal tubular epithelial cells by promoting the expression of mesenchymal phenotype molecules, such as alpha-SMA and collagen I, and down-regulating the expression of epithelial phenotype molecule E-cadherin. Moreover, we have identified the down-regulation of miR-15a which was accompanied with the HG-induced EMT. And the miR-15a overexpression inhibited the alpha-SMA, collagen I expression, and the promotion of E-cadherin expression by targeting and down-regulating AP4 which was also significantly promoted by the HG in the renal tubular epithelial cells. Thus, this study revealed that the weakening regulation on the AP4 expression by miR-15a might contribute to the HG-induced EMT in the renal tubular epithelial cells.
引用
收藏
页码：1363 / 1370
页数：8
相关论文
共 49 条
  • [1] miR-15a and miR-16 Are Implicated in Cell Cycle Regulation in a Rb-Dependent Manner and Are Frequently Deleted or Down-regulated in Non-Small Cell Lung Cancer
    Bandi, Nora
    Zbinden, Samuel
    Gugger, Mathias
    Arnold, Marlene
    Kocher, Verena
    Hasan, Lara
    Kappeler, Andreas
    Brunner, Thomas
    Vassella, Erik
    [J]. CANCER RESEARCH, 2009, 69 (13) : 5553 - 5559
  • [2] MicroRNAs: Target Recognition and Regulatory Functions
    Bartel, David P.
    [J]. CELL, 2009, 136 (02) : 215 - 233
  • [3] MiR-15a and MiR-16 Control Bmi-1 Expression in Ovarian Cancer
    Bhattacharya, Resham
    Nicoloso, Milena
    Arvizo, Rochelle
    Wang, Enfeng
    Cortez, Angelica
    Rossi, Simona
    Calin, George A.
    Mukherjee, Priyabrata
    [J]. CANCER RESEARCH, 2009, 69 (23) : 9090 - 9095
  • [4] A double-negative feedback loop between ZEB1-SIP1 and the microRNA-200 family regulates epithelial-mesenchymal transition
    Bracken, Cameron P.
    Gregory, Philip A.
    Kolesnikoff, Natasha
    Bert, Andrew G.
    Wang, Jun
    Shannon, M. Frances
    Goodall, Gregory J.
    [J]. CANCER RESEARCH, 2008, 68 (19) : 7846 - 7854
  • [5] bantam encodes a developmentally regulated microRNA that controls cell proliferation and regulates the proapoptotic gene hid in Drosophila
    Brennecke, J
    Hipfner, DR
    Stark, A
    Russell, RB
    Cohen, SM
    [J]. CELL, 2003, 113 (01) : 25 - 36
  • [6] Frequent deletions and down-regulation of micro-RNA genes miR15 and miR16 at 13q14 in chronic lymphocytic leukemia
    Calin, GA
    Dumitru, CD
    Shimizu, M
    Bichi, R
    Zupo, S
    Noch, E
    Aldler, H
    Rattan, S
    Keating, M
    Rai, K
    Rassenti, L
    Kipps, T
    Negrini, M
    Bullrich, F
    Croce, CM
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2002, 99 (24) : 15524 - 15529
  • [7] Deregulation of microRNA-503 Contributes to Diabetes Mellitus-Induced Impairment of Endothelial Function and Reparative Angiogenesis After Limb Ischemia
    Caporali, Andrea
    Meloni, Marco
    Voellenkle, Christine
    Bonci, Desiree
    Sala-Newby, Graciela B.
    Addis, Roberta
    Spinetti, Gaia
    Losa, Sergio
    Masson, Rachel
    Baker, Andrew H.
    Agami, Reuven
    le Sage, Carlos
    Condorelli, Gianluigi
    Madeddu, Paolo
    Martelli, Fabio
    Emanueli, Costanza
    [J]. CIRCULATION, 2011, 123 (03) : 282 - U117
  • [8] miR-15 and miR-16 induce apoptosis by targeting BCL2
    Cimmino, A
    Calin, GA
    Fabbri, M
    Iorio, MV
    Ferracin, M
    Shimizu, M
    Wojcik, SE
    Aqeilan, RI
    Zupo, S
    Dono, M
    Rassenti, L
    Alder, H
    Volinia, S
    Liu, CG
    Kipps, TJ
    Negrini, M
    Croce, CM
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2005, 102 (39) : 13944 - 13949
  • [9] Oncogenic HER2δ16 suppresses miR-15a/16 and deregulates BCL-2 to promote endocrine resistance of breast tumors
    Cittelly, Diana M.
    Das, Partha M.
    Salvo, Virgilio A.
    Fonseca, Juan P.
    Burow, Matthew E.
    Jones, Frank E.
    [J]. CARCINOGENESIS, 2010, 31 (12) : 2049 - 2057
  • [10] BTG2 loss and miR-21 upregulation contribute to prostate cell transformation by inducing luminal markers expression and epithelial-mesenchymal transition
    Coppola, V.
    Musumeci, M.
    Patrizii, M.
    Cannistraci, A.
    Addario, A.
    Maugeri-Sacca, M.
    Biffoni, M.
    Francescangeli, F.
    Cordenonsi, M.
    Piccolo, S.
    Memeo, L.
    Pagliuca, A.
    Muto, G.
    Zeuner, A.
    De Maria, R.
    Bonci, D.
    [J]. ONCOGENE, 2013, 32 (14) : 1843 - 1853
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