Search Results
You are looking at 1 - 2 of 2 items for
- Author: R Ann Word x
- Refine by access: All content x
Search for other papers by Charles P Read in
Google Scholar
PubMed
Search for other papers by R Ann Word in
Google Scholar
PubMed
Search for other papers by Monika A Ruscheinsky in
Google Scholar
PubMed
Search for other papers by Brenda C Timmons in
Google Scholar
PubMed
Search for other papers by Mala S Mahendroo in
Google Scholar
PubMed
Cervical remodeling during pregnancy and parturition is a single progressive process that can be loosely divided into four overlapping phases termed softening, ripening, dilation/labor, and post partum repair. Elucidating the molecular mechanisms that facilitate all phases of cervical remodeling is critical for an understanding of parturition and for identifying processes that are misregulated in preterm labor, a significant cause of perinatal morbidity. In the present study, biomechanical measurements indicate that softening was initiated between gestation days 10 and 12 of mouse pregnancy, and in contrast to cervical ripening on day 18, the softened cervix maintains tissue strength. Although preceded by increased collagen solubility, cervical softening is not characterized by significant increases in cell proliferation, tissue hydration or changes in the distribution of inflammatory cells. Gene expression studies reveal a potentially important role of cervical epithelia during softening and ripening in maintenance of an immunomucosal barrier that protects the stromal compartment during matrix remodeling. Expression of two genes involved in repair and protection of the epithelial permeability barrier in the gut (trefoil factor 1) and skin (serine protease inhibitor Kazal type 5) were increased during softening and/or ripening. Another gene whose function remains to be elucidated, purkinje cell protein 4, declines in expression as remodeling progressed. Collectively, these results indicate that cervical softening during pregnancy is a unique phase of the tissue remodeling process characterized by increased collagen solubility, maintenance of tissue strength, and upregulation of genes involved in mucosal protection.
Search for other papers by Beverly G Reed in
Google Scholar
PubMed
Search for other papers by Samir N Babayev in
Google Scholar
PubMed
Search for other papers by Lucy X Chen in
Google Scholar
PubMed
Search for other papers by Bruce R Carr in
Google Scholar
PubMed
Search for other papers by R Ann Word in
Google Scholar
PubMed
Search for other papers by Patricia T Jimenez in
Google Scholar
PubMed
MicroRNAs (miRs) are small molecules important for regulation of transcription and translation. The objective was to identify hormonally regulated miRs in human endometrial stromal cells and to determine the impact of the endocrine disruptor, bisphenol A (BPA), on those miRs. miR microarray analysis and multiple confirmatory cell preparations treated with 17β-estradiol (E2) and BPA altered miR-27b, let-7c, let-7e and miR-181b. Further, decidualization downregulated miR-27b. VEGFB and VEGFC were validated as targets of miR-27b. Identification of miR-27b target genes suggests that BPA and E2 downregulate miR-27b thereby leading to upregulation of genes important for vascularization and angiogenesis of the endometrium during the menstrual cycle and decidualization.
