Uterine Deletion of Trp53 Compromises Antioxidant Responses in the Mouse Decidua

Overview

Journal Endocrinology

Publisher Oxford University Press

Specialty Endocrinology

Date 2012 Jul 5

PMID 22759378

Citations 22

Authors

Kristin E Burnum

Yasushi Hirota

Erin S Baker

Mikihiro Yoshie

Yehia M Ibrahim

Matthew E Monroe

Gordon A Anderson

Richard D Smith

Takiko Daikoku

Sudhansu K Dey

Affiliations

Soon will be listed here.

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.

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