Ramkumar Menon,
Distinguished John D. Stobo, MD, Endowed Chair and Professor,
The University of Texas Medical Branch (UTMB)
Dr. Ramkumar Menon is a tenured Professor in the Department of Obstetrics and Gynecology/Cell biology at the University of Texas Medical Branch at Galveston, TX. He is also the Director of the Division of Basic Science and Translational Research at UTMB. The primary focus of his lab is to design strategies to reduce PTB risk using extracellular vesicles as a drug delivery vehicle to treat the fetal inflammatory response. His lab develops various Organ-on-Chip models for various intrauterine organ systems. His research is funded by multiple grants from the National Institute of Health (NIH, USA) and other non-federal agencies. He has published over 300 peer-reviewed articles and book chapters. Dr. Menon has mentored over 30 medical and postgraduate students. Dr. Menon is also the executive director of Preterm birth International Collaborative, not-for-profit research and educational organization involved in preterm birth research.
Modeling the Feto-Maternal Communication by Extracellular Vesicles using Intrauterine Tissue Microphysiologic System
Tuesday, 20 June 2023 at 11:30
Add to Calendar ▼2023-06-20 11:30:002023-06-20 12:30:00Europe/LondonModeling the Feto-Maternal Communication by Extracellular Vesicles using Intrauterine Tissue Microphysiologic SystemCirculating Biomarkers and Extracellular Vesicles Europe 2023 in Rotterdam, The NetherlandsRotterdam, The NetherlandsSELECTBIOenquiries@selectbiosciences.com
The fetal inflammatory response in response to intrauterine inflammation is a major determinant of adverse pregnancy outcomes, specifically preterm birth (PTB). Inflammation causes intrauterine tissue (fetal membrane/amniochorion) senescence and generate damage-associated molecular pattern markers (e.g., High mobility group box 1 protein [HMGB1]). HMGB1 is released via extracellular vesicles. We tested the hypothesis that exosomal HMGB1 is one of the fetal signals capable of increasing Feto-Maternal interface (FMi) inflammation, predisposing to PTB. To test this hypothesis, exosomes from amnion epithelial cells (AECs) from the intrauterine fetal membranes grown under normal conditions were engineered to contain HMGB1 by (eHMGB1). eHMGB1 was characterized, and its propagation through FMi was tested using a four-chamber microfluidic organ-on-a-chip device (FMi-OOC) that contained four distinct cell types (amnion epithelium, amnion mesenchyme, chorion trophoblast and decidual cells) connected through microchannels. eHMGB1 propagated through the fetal cells to the maternal decidua and increased inflammation associated with PTB. To physiologically validate this finding, eHMGB1(containing 10 ng) was intra-amniotically injected into CD-1 mice on embryonic day 17 which resulted in PTB. In vivo kinetics was determined by injecting carboxyfluorescein succinimidyl ester labeled eHMGB1. We report that eHMGB1 trafficking in mice causing PTB was associated with increased FMi inflammation. Our study determined that fetal exosome-mediated paracrine signaling can generate inflammation and induce parturition.
Add to Calendar ▼2023-06-19 00:00:002023-06-20 00:00:00Europe/LondonCirculating Biomarkers and Extracellular Vesicles Europe 2023Circulating Biomarkers and Extracellular Vesicles Europe 2023 in Rotterdam, The NetherlandsRotterdam, The NetherlandsSELECTBIOenquiries@selectbiosciences.com
Add to Calendar ▼2023-06-20 11:30:002023-06-20 12:30:00Europe/LondonModeling the Feto-Maternal Communication by Extracellular Vesicles using Intrauterine Tissue Microphysiologic SystemCirculating Biomarkers and Extracellular Vesicles Europe 2023 in Rotterdam, The NetherlandsRotterdam, The NetherlandsSELECTBIOenquiries@selectbiosciences.com
