Biomechanical function of the murine cervix with elastic fiber deficiency.

Preterm birth (PTB) is the leading cause of infant death globally. Improper softening and dilation of the cervix due to cervical insufficiency is a major contributor to PTB. However, the processes describing why or how the cervix prematurely remodels are not well understood. Elastic fibers and smooth muscle cells contribute to contractile and mechanical stability in soft tissues, but their relationship in the cervix is not fully characterized. Towards this end, this study uses the fibulin-5 global knockout mouse model to investigate the impact of elastic fiber deficiency on the contractile and biomechanical behavior of the cervix. Cervixes from nulliparous fibulin-5 wildtype (Fbln5+/+), haploinsufficient (Fbln5+/-), and deficient (Fbln5-/-) mice were explanted and subjected to biaxial contractile and biomechanical extension-inflation testing. Immunofluorescence was used to quantify the localization and expression of elastin and alpha-smooth muscle actin throughout the cervix. Elastin expression and the number of elastic fibers decreased with Fbln5 deficiency. Additionally, contractility and modulus were significantly reduced in the Fbln5-/- cervix as a consequence of elastic fiber deficiency. Overall, this study showed that intact elastic fibers significantly contribute to biomechanical function of the cervix and may be an essential target for future PTB investigations.