title: Uterine deletion of Trp53 compromises antioxidant responses in the mouse decidua.
abstract: 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.
authors: Biological Sciences Division, Pacific Northwest National Laboratory, Richland, Washington 99352-9104, USA.
authors: Kristin E
authors: KE
authors: Burnum
authors: Yasushi
authors: Y
authors: Hirota
authors: Erin S
authors: ES
authors: Baker
authors: Mikihiro
authors: M
authors: Yoshie
authors: Yehia M
authors: YM
authors: Ibrahim
authors: Matthew E
authors: ME
authors: Monroe
authors: Gordon A
authors: GA
authors: Anderson
authors: Richard D
authors: RD
authors: Smith
authors: Takiko
authors: T
authors: Daikoku
authors: Sudhansu K
authors: SK
authors: Dey
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D003656:Decidua / Q000378:metabolism*; D005260:Female; D051379:Mice; D018384:Oxidative Stress / Q000235:genetics; D047928:Premature Birth / Q000235:genetics / Q000378:metabolism; D016159:Tumor Suppressor Protein p53 / Q000172:deficiency* / Q000235:genetics; D014599:Uterus / Q000378:metabolism*
chemical_list: D000975:Antioxidants; D016159:Tumor Suppressor Protein p53