alexa Molecular Analysis of Implantation Defects in Homeobox Gene Hoxa10-Deficient Mice
ISSN: 2161-038X

Reproductive System & Sexual Disorders: Current Research
Open Access

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Research Article

Molecular Analysis of Implantation Defects in Homeobox Gene Hoxa10-Deficient Mice

Yan Yin1, Congxing Lin1, Dima Sawalha1, Brent M. Bany3 and Liang Ma1,2*

1Division of Dermatology, Department of Medicine, Washington University School of Medicine, 660 S. Euclid Avenue, St. Louis, MO 63110, USA

2Department of Developmental Biology, Washington University School of Medicine, 660 S. Euclid Avenue, St. Louis, MO 63110, USA

3Department of Ophthalmology, Faculty of Medicine Ankara University, Turkey

Corresponding Author:
Liang Ma
Division of Dermatology
Department of Medicine Washington University
Campus Box 8123, 660 South Euclid Avenue
St. Louis, MO 63110, USA
Tel: (314) 454-8771
Fax: (314) 454-5626
Email: [email protected]

Received Date: October 17, 2011; Accepted Date: November 16, 2011; Published Date: November 18, 2011

Citation: Yin Y, Lin C, Sawalha D, Bany BM, Ma L (2011) Molecular Analysis of Implantation Defects in Homeobox Gene Hoxa10-Deficient Mice. Reproductive Sys Sexual Disord S1:001. doi:10.4172/2161-038X.S1-001

Copyright: © 2011 Yin Y, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.



The success of embryo implantation depends on the receptivity of the uterus. Abdominal B class homeobox gene Hoxa10 is dynamically expressed around implantation, and is indispensable for establishing uterine receptivity. However, the exact mechanism through which HOXA10 exerts its function remains elusive. In this report, we investigated the molecular basis for the implantation failure caused by Hoxa10 deficiency using both knock-out mouse models and global gene expression profiling approaches. We demonstrated that augmented local immune response through T/B cells alone is not sufficient to explain the implantation defects observed in the Hoxa10-null uterus. We also uncovered a group of potential genes and signaling pathways that may participate in the downstream events mediated by HOXA10.

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