Jada Okaikoi
MIT Department: Biological Engineering
Faculty Mentor: Prof. Linda Griffith
Research Supervisor: Laura Bahlmann
Undergraduate Institution: University of Nevada, Reno
Hometown: Las Vegas, Nevada
Website: LinkedIn
Biography
Jada Okaikoi is an undergraduate Biomedical Engineering student at the University of Nevada Reno. She will graduate in May 2025 as an Honors, McNair, and Maximizing Access to Research Careers (MARC) scholar. At her home institution, Jada investigates fibrin’s effects on 3D bioengineered uterine smooth muscle as a suitable in vitro model for pre-term labor drug discovery in Professor Heather Burkin’s lab. She is a recipient of the Nevada Undergraduate Research Award for the Summer/Fall 2023 award period and the Fall 2024 award period. Currently, Jada is conducting endometriosis research in Professor Linda Griffith’s lab at MIT through the Summer Research Program. Her research focuses on parsing the effects of c-Jun kinase inhibitors’ inflammatory responses in endometrial stromal cells, toward advancing drug treatment options for endometriosis.
Abstract
Effect of c-Jun Kinase Inhibitors on Decidualization and
Inflammatory Response of Endometrial Stromal Cells
Jada Okaikoi1, Laura Bahlmann2, Stephen Palmer3, Douglas Lauffenburger2 and
Linda Griffith2
1Department of Biomedical Engineering, University of Nevada Reno
2Department of Biological Engineering, Massachusetts Institute of Technology
3Baylor College of Science
Endometriosis, affecting 10% of girls and women worldwide, involves the growth of
endometrial tissue outside the uterus, leading to chronic inflammation and other symptoms.
Recent studies in animal models have demonstrated that c-Jun kinase inhibitors (JNKi) can
decrease the size and volume of endometriosis lesions; however, the effect of JNKi on
patients remains unclear due to a lack of relevant models. We quantified the effects of five
c-Jun kinase inhibitors on patient endometrial stromal cells (ESCs) isolated from biopsies
collected during surgical procedures. ESCs were stimulated with progesterone or IL1-β (to
induce inflammation) and treated with the drugs. Media was collected and prolactin, IL8,
and IL6 were analyzed using enzyme-linked immunosorbent assays. Preliminary results
indicate that each drug has nuanced effects on ESC phenotype. Future work will focus on
the investigation of these drug compounds in our humanized lesion models of endometriosis.
