Uterine Deletion of Trp53 Compromises Antioxidant Responses in the Mouse Decidua

被引:29
作者
Burnum, Kristin E. [2 ]
Hirota, Yasushi [1 ]
Baker, Erin S. [2 ]
Yoshie, Mikihiro [1 ]
Ibrahim, Yehia M. [2 ]
Monroe, Matthew E. [2 ]
Anderson, Gordon A. [2 ]
Smith, Richard D. [2 ]
Daikoku, Takiko [1 ]
Dey, Sudhansu K. [1 ]
机构
[1] Univ Cincinnati, Cincinnati Childrens Hosp Med Ctr, Coll Med, Div Reprod Sci,Perinatal Inst, Cincinnati, OH 45229 USA
[2] Pacific NW Natl Lab, Div Biol Sci, Richland, WA 99352 USA
基金
美国国家卫生研究院; 日本学术振兴会;
关键词
MITOCHONDRIAL-DNA MUTATIONS; ENDOMETRIAL STROMAL CELLS; OXIDATIVE STRESS; PRETERM BIRTH; IN-VITRO; SOFTWARE PACKAGE; TUMOR-SUPPRESSOR; LIFE-SPAN; PREGNANCY; MASS;
D O I
10.1210/en.2012-1335
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Preterm birth is a global health issue impacting millions of mothers and babies. However, the etiology of preterm birth is not clearly understood. Our recent finding that premature decidual senescence with terminal differentiation is a cause of preterm birth in mice with uterine Trp53 deletion, encoding p53 protein, led us to explore other potential factors that are related to preterm birth. Using proteomics approaches, here, we show that 183 candidate proteins show significant changes in deciduae with Trp53 deletion as compared with normal deciduae. Functional categorization of these proteins unveiled new pathways that are influenced by p53. In particular, down-regulation of a cluster of antioxidant enzymes in p53-deficient deciduae suggests that increased oxidative stress could be one cause of preterm birth in mice harboring uterine deletion of Trp53. (Endocrinology 153: 4568-4579, 2012)
引用
收藏
页码:4568 / 4579
页数:12
相关论文
共 49 条
[41]   Cre-mediated recombination in cell lineages that express the progesterone receptor [J].
Soyal, SM ;
Mukherjee, A ;
Lee, KYS ;
Li, J ;
Li, HG ;
DeMayo, FJ ;
Lydon, JP .
GENESIS, 2005, 41 (02) :58-66
[42]   Evidence for coordinated interaction of cyclin D3 with p21 and cdk6 in directing the development of uterine stromal cell decidualization and polyploidy during implantation [J].
Tan, J ;
Raja, S ;
Davis, MK ;
Tawfik, O ;
Dey, SK ;
Das, SK .
MECHANISMS OF DEVELOPMENT, 2002, 111 (1-2) :99-113
[43]   Functions of alpha 2 macroglobulins in pregnancy [J].
Tayade, C ;
Esadeg, S ;
Fang, Y ;
Croy, BA .
MOLECULAR AND CELLULAR ENDOCRINOLOGY, 2005, 245 (1-2) :60-66
[44]   p53, ROS and senescence in the control of aging [J].
Vigneron, Arnaud ;
Vousden, Karen H. .
AGING-US, 2010, 2 (08) :471-474
[45]   Surfing the p53 network [J].
Vogelstein, B ;
Lane, D ;
Levine, AJ .
NATURE, 2000, 408 (6810) :307-310
[46]   MITOCHONDRIAL-DNA MUTATIONS IN HUMAN DEGENERATIVE DISEASES AND AGING [J].
WALLACE, DC ;
SHOFFNER, JM ;
TROUNCE, I ;
BROWN, MD ;
BALLINGER, SW ;
CORRALDEBRINSKI, M ;
HORTON, T ;
JUN, AS ;
LOTT, MT .
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE, 1995, 1271 (01) :141-151
[47]   Akt as a possible intracellular mediator for decidualization in human endometrial stromal cells [J].
Yoshino, O ;
Osuga, Y ;
Hirota, Y ;
Koga, K ;
Yano, T ;
Tsutsumi, O ;
Taketani, Y .
MOLECULAR HUMAN REPRODUCTION, 2003, 9 (05) :265-269
[48]   Mitochondrial impairment in p53-deficient human cancer cells [J].
Zhou, S ;
Kachhap, S ;
Singh, KK .
MUTAGENESIS, 2003, 18 (03) :287-292
[49]   Advances in proteomics data analysis and display using an accurate mass and time tag approach [J].
Zimmer, JSD ;
Monroe, ME ;
Qian, WJ ;
Smith, RD .
MASS SPECTROMETRY REVIEWS, 2006, 25 (03) :450-482