NDLI: Overexpression of Uromodulin-like1 accelerates follicle depletion and subsequent ovarian degeneration.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Wang, W. Tang, Y. Ni, L. Kim, E. Jongwutiwes, T. Hourvitz, A. Zhang, R. Xiong, H. Liu, H-C Rosenwaks, Z.
Description	Country affiliation: United States Author Affiliation: Wang W ( The Ronald O. Perelman and Claudia Cohen Center for Reproductive Medicine, Weill Medical College of Cornell University, New York, NY 10065, USA. wew2004@med.cornell.edu)
Abstract	Murine Uromodulin-like 1 (Umodl1) encodes Ca(2+)-dependent EGF-like membrane-bound proteins. This study presents its novel expression in the immune and female reproductive systems. Upon stimulation by CD3/CD28 antibodies, Umodl1 showed a prompt and robust response in the proliferating CD4(+) T cells, suggesting its implication in immune defense against pathogens. In ovary, Umodl1 is regulated by gonadotropins. Mice carrying extra copies of functional Umodl1 were generated by BAC transgenesis. Defects in the female reproductive system became evident from 4 months of age, manifested by reduced or diminished fertility. Histology revealed that the ovaries contained very few discernible follicles in the cortical region, and were devoid of distinguishable corpus lutea (CL). Among the multilayered preantral follicles, elevated apoptosis was observed in both the oocytes and surrounding granulosa cells (GCs). Furthermore, a high level of PPARÎ³ indicated an abnormal adipogenesis in the mutant ovaries, which resulted in the conversion of GCs into adipocytes. By 6 months of age, all mutant mice became anovulatory. Ovarian tissues including CL, follicles of various stages and associated stromal cells were degenerated. Altered expression of AMH, follicle-stimulating hormone and other ovary-specific marker genes such as Gdf-9, Rnf35, NOHLH and Gcx-1 further demonstrated that the molecular properties of the mutant ovaries have been severely disturbed. This work presents a novel animal model for investigating the pathogenesis of premature ovarian failure or early ovarian ageing.
File Format	HTM / HTML
e-ISSN	20414889
DOI	10.1038/cddis.2012.169
Journal	Cell Death and Disease
Volume Number	3
Language	English
Publisher	Nature Publishing Group
Publisher Date	2012-11-29
Publisher Place	Great Britain (UK)
Access Restriction	Open
Subject Keyword	Ovarian Follicle Research Support, Non-u.s. Gov't Anovulation Gene Expression Calcium-binding Proteins Cytology Mice, Transgenic Metabolism Physiopathology Membrane Proteins Discipline Cell Biology Ovary Animals Primary Ovarian Insufficiency Genetics Mice Corpus Luteum Apoptosis Disease Models, Animal
Content Type	Text
Resource Type	Article

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