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This Article Full Text Full Text (PDF) All Versions of this Article: 73/3/472    most recent biolreprod.105.041855v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal My Folders Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Velarde, M. C. Articles by Simmen, R. C.M. Search for Related Content PubMed PubMed Citation Articles by Velarde, M. C. Articles by Simmen, R. C.M. Agricola Articles by Velarde, M. C. Articles by Simmen, R. C.M.

Null Mutation of Krüppel-Like Factor9/Basic Transcription Element Binding Protein-1 Alters Peri-Implantation Uterine Development in Mice¹

Department of Physiology and Biophysics,³ University of Arkansas for Medical Sciences Arkansas Children's Nutrition Center,⁴ Little Rock, Arkansas 72202

Female mice null for the basic transcription element binding protein-1 (Bteb1) gene have reduced numbers of implanting embryos. We hypothesized that the implantation defect, resulting in subfertility, is a consequence of developmental asynchrony between the embryo and uterine endometrium at peri-implantation. To address this, endometrium from wild-type (WT) and Bteb1^(–/–) females at 0.5 to 5.5 days postcoitum (dpc) were evaluated for proliferation (BrdU labeling), apoptosis (TUNEL), and steroid hormone receptor expression (immunohistochemistry). Loss of BTEB1 did not affect serum estrogen (E) and progesterone (P) levels. In stroma (ST), the numbers of progesterone receptor (PGR) and HomeoboxA10 (HOXA10)-expressing cells were lower (3.5 and 4.5 dpc), while those of estrogen receptor-alpha (ESR1) were higher (3.5 dpc), with Bteb1 ablation. The peak of proliferation in luminal epithelium (LE), glandular epithelium (GE), and ST was delayed, while the apoptotic index in all cell types was increased (2.5 dpc) in Bteb1^(–/–) relative to WT mice. The numbers of PGR-positive ST cells was negatively correlated with LE proliferation in WT mice; this correlation was lost in Bteb1^(–/–) mice and was not observed before 2.5 dpc for both genotypes. Proliferation and apoptosis in all endometrial compartments, as well as the numbers of PGR-, HOXA10-, and ESR1-expressing ST cells, were lower in Bteb1^(–/–) relative to WT mice after ovariectomy and E + P treatment. Results suggest that BTEB1, by regulating ST PGR expression and transactivation, participates in the paracrine control of LE proliferation by PGR and thus is important for establishment of a receptive uterus critical for successful implantation.

female reproductive tract, implantation, progesterone, steroid hormone receptors, uterus

² Correspondence: Rosalia C.M. Simmen, University of Arkansas for Medical Sciences and Arkansas Children's Nutrition Center, 1120 Marshall St., Little Rock, AR 72202. FAX: 501 364 3161; simmenrosalia{at}uams.edu

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