Reproductive success requires accurately timed remodeling of the cervix to orchestrate the maintenance of pregnancy, the process of labor, and birth. Prior work in mice established that a combination of continuous turnover of fibrillar collagen and reduced formation of collagen cross-links allows for the gradual increase in tissue compliance and delivery of the fetus during labor. However, the mechanism for continuous collagen degradation to ensure turnover during cervical remodeling is still unknown.
View Article and Find Full Text PDFBackground: Maternal high fat diet (mHFD) exposure expands IL-17 producing group 3 innate lymphoid cells (IL17 ILC3) in the small intestine of neonatal murine offspring and increases their susceptibility to intestinal inflammation. How mHFD modulates innate immunity in the fetal offspring remains unclear.
Methods: Dams were exposed to 60% high fat diet or maintained on regular diet (RD) prior to and during mating.
Uterine cervical remodeling is a fundamental feature of pregnancy, facilitating the delivery of the fetus through the cervical canal. Yet, we still know very little about this process due to the lack of methodologies that can quantitatively and unequivocally pinpoint the changes the cervix undergoes during pregnancy. We utilize polarization-resolved second harmonic generation to visualize the alterations the cervix extracellular matrix, specifically collagen, undergoes during pregnancy with exquisite resolution.
View Article and Find Full Text PDFEstradiol (E2) and relaxin (Rln) are steroid and polypeptide hormones, respectively, with important roles in the female reproductive tract, including myometrium. Some actions of Rln, which are mediated by its membrane receptor RXFP1, require or are augmented by E2 signaling through its cognate nuclear steroid receptor, estrogen receptor alpha (ERα). In contrast, other actions of Rln act in opposition to the effects of E2.
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