Hi everyone! My name is Lorena Ye, and I am a rising senior at the Dietrich School of Arts and Sciences. I am majoring in Biochemistry with minors in Computer Science and Chemistry and a certificate in Global Health. Outside of school, I love working out, running, and crocheting. I also help run Pitt’s chapter of Bridge Beyond, a national nonprofit that provides resources to people experiencing homelessness. When I’m not occupied with school and outside interests, you can probably find me in the research lab!

This summer, I am super excited to conduct meaningful research alongside my peers through the Health Sciences Fellowship. For the past two years, I’ve been working in Dr. Evan Ray’s lab in the Renal-Electrolyte Division of Pitt’s Department of Medicine. During much of my time here, I have been investigating renal magnesium (Mg²⁺) handling in lactation. One of the kidney’s vital functions is to maintain bodily homeostasis by reabsorbing essential nutrients back into the bloodstream. While there are hormones known to participate in calcium, sodium, and potassium regulation in the kidney, we still don’t know of any hormone directly involved in renal Mg²⁺ balance. My overarching project seeks to address this gap by examining potential mechanisms for Mg²⁺conservation by the kidney. Laboratory techniques I commonly use include immunofluorescence staining in kidney tissue or cells, cryosectioning, and Western blots.

To investigate how the kidney adapts to extreme Mg²⁺ depletion, we are using the model of lactation in mice. You might be wondering how exactly lactation is connected to magnesium levels in the body. Here’s the answer: our bones are primarily composed of calcium (Ca²⁺) and magnesium. When a female mammal is lactating, she delivers a large amount of her own bone minerals to her offspring through her breastmilk, which means her Mg²⁺ (and Ca²⁺) stores become severely depleted. Her kidneys, gastrointestinal tract, and other organs work to compensate for this extreme mineral loss. Previous data in mice and humans show that Mg²⁺ excretion in the urine is decreased in lactating females, making lactation a favorable model to study Mg²⁺ regulation by the kidney. We’ve also observed that mRNA transcript levels of Trpm6, a gene encoding a Mg²⁺-selective transporter, increase significantly in lactation. These data led us to ask the question: How does the kidney upregulate Trpm6 levels during lactation? Through the Health Sciences Fellowship this summer, I will explore this question by examining lactation-associated changes in kidney tubule morphology, specifically the tubule segment in which Trpm6 is expressed. Our logic is that an upregulation in Trpm6 message could result from increased size of the tubule segment expressing Trpm6, either through an increase in cell size or in cell number.

I feel that my research is important because it is part of a larger effort to develop a novel mechanism for Mg²⁺ regulation in the body. My work will also have implications on physiological disorders characterized by electrolyte imbalances, such as hypertension, diabetes, and heart disease. Over the past two years, my experiences in the lab have solidified my determination to pursue higher education and eventually a career in research. As someone who is deeply passionate about the biomedical applications of research, I plan to pursue a doctoral degree in the biomedical sciences. Being able to articulate my science to people of varying academic backgrounds is a crucial skill that will aid me in my graduate studies and beyond. Therefore, participating in the Health Sciences Fellowship will bring me closer to my goals by encouraging my collaboration with people of different disciplines and communication of my research to a wider audience. I look forward to a summer of collaboration, experimentation, and growth!