Investigating the interactions of mechanical forces and hormones on ECM synthesis

Conventional wisdom states that adult cells do not produce elastin; however, this is not the case in uterus during pregnancy. In the third trimester, the same time that fetal elastin is produced, the myometrial layer of the uterus increases in elastin content by at least 5-fold. Postpartum, much of the elastin is degraded with the overall content returning to pre-pregnancy levels. During the third trimester there is a significant increase in estrogen and progesterone levels as well as significant mechanical stretch due to fetal growth and movement. The long-term goals of this project are to identify mechanisms by which we can induce elastin synthesis from many adult cell types for tissue-engineering and wound healing applications. To achieve this we must first identify potential mechanisms behind elastin synthesis in the known elastin producing cells. These mechanisms can then be validated to determine their effect on elastin or production of other extracellular matrix proteins.

Illustration of elastin's structure

Figure 1: A) Basic structure of elastin. It is the elastic component of many tissues allowing them to retain their shape. B) Plasma hormone levels in pregnant females. Estrogens and progesterone are significantly elevated compared to non-pregnant levels


Headshot of Stacey Colleen Schutte

Stacey Colleen Schutte

Assistant Professor, CEAS - Biomedical Eng



Research areas: Engineering of soft tissue including skin, elastin synthesis, mechanobiology, and effects of proteases on wound healing.