Katie Seu, PhD

My research aims to identify and investigate molecular pathways essential for red blood cell production and function. My interest in red blood cells began as a graduate student in the lab of Dr. Phil Low at Purdue University, where I investigated the regulation of red blood cell deformability. I became fascinated by how specialized and unique these cells are in order to perform the essential task of transporting oxygen throughout the body. The human body produces over two million red blood cells per second to maintain homeostasis, yet there is still so much that we need to learn about how red cells are made and why this goes wrong in some patients. By uncovering the molecular mechanisms that lead to erythropoiesis disorders, such as congenital dyserythropoietic anemia, we can identify therapeutic targets to help treat and manage these and other blood disorders.

After obtaining my PhD, I came to Cincinnati Children's as a postdoctoral fellow to work with Dr. Theodosia Kalfa and began studying the cell-extrinsic requirements for erythropoiesis in the erythroblastic island (EBI) niche and its involvement in anemia of inflammation. I developed and published a method to analyze EBIs from mouse tissues using imaging flow cytometry that is now used widely by other researchers in the field. Using this method, we identified that myeloid cells, commonly found in EBIs, are maturing granulocytic precursors and demonstrated that they mature parallel to erythroblasts within this common niche (erythro-myeloblastic islands, EMBIs). Our article was featured on the cover of Blood in an October 2022 issue with an image I took of one such EMBI. This work has implications for anemia of inflammation, a serious complication of chronic diseases affecting millions worldwide.

Following the creation of the Congenital Dyserythropoietic Anemia (CDA) registry by Dr. Kalfa in 2016, I became interested in the cell-intrinsic aspects of erythropoiesis and began investigating the mechanisms of CDA pathogenesis. Together, we uncovered a syndromic type of CDA caused by mutations in a protein called VPS4A, which is critical for proper cell division and endocytic trafficking. To demonstrate the pathogenesis of these VPS4A mutations, I established an ex vivo erythropoiesis culture system to study defects in erythroblasts produced from patient-derived induced pluripotent stem cells (iPSCs). Now, as a research assistant professor at Cincinnati Children's, my lab is focused on investigating the role of vesicle trafficking in erythropoiesis and red cell maturation to advance our understanding and treatment of erythropoiesis disorders.

I have been a researcher for over 11 years and began working at Cincinnati Children's in 2013.