Desmosine Content and Passive Mechanics of the Elastic Fiber Deficient Murine Uterus

Abstract

Elastic fibers in the extracellular matrix provide compliance and distensibility to soft biological tissues, such as the uterus. The uterus grows and remodels during processes such as gestation and menstruation. Preterm birth may be associated with uterine overdistention, which can be exacerbated in females with underdeveloped elastic fibers. Desmosine crosslinks form between mature elastic fibers and can be used to infer the mature fiber content. Fibulin-5 (Fbln5) is expressed in tissues abundant in elastic fibers, and mice deficient in Fbln5 develop pelvic floor disorders similar to females with genetic disorders that negatively impact elastic fiber formation. Prior work has quantified desmosine content to study elastic fiber turnover in the vagina of Fbln5 deficient mice. However, the presence of mature elastic fibers in uterine tissue with varying Fbln5 expression is unknown. Further, the influence of desmosine content on passive uterine mechanics is unknown. Therefore, the objective of this study was to determine the role of Fbln5 insufficiency on desmosine content and its effect on passive mechanics of the murine uterus. We hypothesize that Fbln5 haploinsufficient and deficient murine uterine tissue will have lower desmosine content than wildtype tissue. It is further hypothesized that Fbln5 haploinsufficiency or deficiency will decrease the passive compliance and distensibility of the murine uterus. Characterizing the desmosine content and passive distensibility of the murine uterus may provide insight into the influence of elastic fiber deficiency on uterine function, which can be applied to the clinical setting to assess the etiology of pelvic floor disorders in women with disrupted elastic fiber development.