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Nuclear receptor co-regulator Krüppel-like factor 9 and prohibitin 2 expression in oestrogen-induced epithelial cell proliferation in the mouse uterus

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Nuclear receptor co-regulator Krüppel-like factor 9 and prohibitin 2 expression in oestrogen-induced epithelial cell proliferation in the mouse uterus

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Pabona, J. M. P. Velarde, M. C. Zeng, Z. Simmen, F. A. Simmen, R. C. M.
Description	Country affiliation: United States Author Affiliation: Pabona JM ( Department of Physiology and Biophysics, University of Arkansas for Medical Sciences and Arkansas Children's Nutrition Center, Little Rock, Arkansas 72202, USA.)
Abstract	Oestrogen, acting through its cognate receptor oestrogen receptor-α (ERα), is a critical regulator of uterine endometrial epithelial proliferation. Although the dynamic communication between endometrial stromal and epithelial cells is considered to be an important component in this process, key molecular players in particular compartments remain poorly defined. Here, we used mice null for Krüppel-like factor 9 (KLF9) to evaluate the contribution of this nuclear protein in stromal-epithelial interactions underlying proliferative effects of oestrogen. We find that in ovariectomized mice administered estradiol-17β $(E_{2})$ for 24 h, Klf9 null mutation resulted in lack of $E_{2}-induced$ proliferative response in all endometrial compartments. We demonstrate a negative association between Klf9 expression and nuclear levels of ERα transcriptional corepressor prohibitin (PHB) 2 in uterine stromal and epithelial cells of $E_{2}-treated$ wildtype (WT) and Klf9 null mice. In early pregnancy uteri of WT mice, the temporal pattern of Klf9 transcript levels was inversely associated with that of Phb2. Deletion of Klf9 up-regulated uterine Phb2 expression and increased PHB2 nuclear localization in endometrial stromal and epithelial cells, with no effects on the expression of the related Phb1. In the human endometrial stromal cell line HESC treated with $E_{2}$ for 24 h, KLF9 siRNA targeting augmented PHB2 transcript and increased nuclear PHB2 protein levels, albeit this effect was not to the extent seen in vivo with Klf9 null mutants. Our findings suggest a novel mechanism for control of oestrogen-induced luminal epithelial proliferation involving stromal KLF9 regulation of paracrine factor(s) to repress epithelial expression of corepressor PHB2.
File Format	HTM / HTML
ISSN	00220795
e-ISSN	14796805
DOI	10.1677/JOE-08-0383
Journal	Journal of Endocrinology
Issue Number	1
Volume Number	200
Language	English
Publisher	BioScientifica
Publisher Date	2009-01-01
Publisher Place	Great Britain (UK)
Access Restriction	Open
Subject Keyword	Discipline Endocrinology Cell Proliferation Epithelial Cells Cytology Estrogens Metabolism Gene Expression Kruppel-like Transcription Factors Repressor Proteins Uterus Animals Cell Nucleus Endometrium Estradiol Estrogen Receptor Alpha Genetics Mice Protein Binding Research Support, N.i.h., Extramural
Content Type	Text
Resource Type	Article
Subject	Endocrinology, Diabetes and Metabolism Endocrinology

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Nuclear receptor co-regulator Krüppel-like factor 9 and prohibitin 2 expression in oestrogen-induced epithelial cell proliferation in the mouse uterus

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