What was your research hypothesis or goal?

My research focused on the Planar Cell Polarity pathway with two goals in mind. First I wanted to show that intestinal epithelium uses the PCP pathway to coordinate cellular migration. Second, I sought to build a mathematical model of PCP protein interactions, to understand how the individual protein interactions in the pathway work together to form tissue level cell polarity.

What were the major findings from your PhD research?

We found that PCP had a strong role in controlling intestinal migration, and that a recently identified set of localized PCP phosphorylation reactions is a sufficient mechanism to drive known tissue-level PCP phenotypes.

What is your career goal and what are you doing next?

I am starting my own business, providing researchers with a wide array of computational bioscience services.

What was your research hypothesis or goal?

We hypothesized that class I electrophilic Nrf2 activators suppress neointimal hyperplasia (NH) by inhibiting the proliferation, migration, and phenotypic modulation of vascular smooth muscle cells.

What were the major findings from your PhD research?

Nrf2 activation increases antioxidant enzyme expression and prevents VSMCs from switching to a disease-linked “synthetic” state. In animal models, we showed that periadventitial delivery of these activators significantly reduced arterial and venous stenosis.

What is your career goal and what are you doing next?

I am excited to transition into the biotechnology and dental industries, where I can use my clinical background and research skills to support strategic business growth and the development of next generation therapies.

What was your research hypothesis or goal?

The central question of my work was: “why do some immunotherapies fail in solid cancers?”. We focused on T cells which infiltrate tumors and destroy cancer cells – I hypothesized that the hostile environment of the solid tumor alters the cell biology of T cells, and asked if preventing those changes to the T cell could improve immunotherapy.

What were the major findings from your PhD research?

I studied T cells, the main immune cell that fights against cancer in immunotherapy. When looking at these T cells taken from cancer patients, I found that the endoplasmic reticulum (an organelle where a lot of protein is made) becomes enlarged due to the upregulation of a structural protein called CKAP4. This enlargement happens in hypoxic environments, which are commonly found in solid tumors. Excitingly, we could limit this enlargement from occurring by adding inhibitors to cell stress or removing the CKAP4 gene from cells. These treatments enabled the cell to make much more protein and were superior at controlling tumor growth in mice.

What is your career goal and what are you doing next?

My real passion lies in taking what we learn at the bench and actually getting it to patients. Lately, I’ve realized that I can make the biggest difference by focusing on the business side of science to actually bring these discoveries to the clinic, though I’m still keeping a few different doors open. For now, I’m staying on as a postdoc in Jessica Thaxton’s lab to continue my research while I map out my next steps.

What was your research hypothesis or goal?

My research goal is to understand how different type of renal nerves innervate the kidney, establish neuro-effector junctions and innervated developing renal structures. In addition, we aim to understand how renal nerve mediate kidney development and impact renal function.

What were the major findings from your PhD research?

In our study, we provided a comprehensive, high-resolution map of sensory and sympathetic innervation in the developing mouse kidney, offering critical insights into how renal neural networks are established during organogenesis and postnatal maturation. We delineate the spatial and temporal dynamics of distinct nerve populations, revealing that renal innervation begins in concert with arterial differentiation and progressively innervate with nephrons during development. We established the conserved innervation patterns in both mouse and human kidneys underscoring their physiological relevance. Moreover, renal nerves establish neuroeffector junctions with kidney structures during development. Finaly, we showed that in utero renal denervation leads to lower number of nephrons during development. This established that nerve-derived paracrine cues modulate nephrogenesis, revealing bidirectional signaling crosstalk between peripheral nerves and the developing renal tissue.

What is your career goal and what are you doing next?

My hope is to continue to grow and improve as a scientist and in life. In my next position, I will be continuing research and making scientific discoveries at the University of Pennsylvania in the Laboratory of Dr. Alex Hughes, where I will be studying tissue engineering and renal development.

What was your research hypothesis or goal?

My research goal was to investigate the role of RAPGEF2, a previously uncharacterized RAP-GEF in platelets, in RAP1-mediated integrin activation in platelets, and how RAPGEF2 contributes to hemostasis and thrombosis.

What were the major findings from your PhD research?

We found that RAPGEF2 is indeed important for RAP1-mediated integrin activation, and that RAPGEF2 operates downstream of G13-coupled receptors. We also found that RAPGEF2 is important for hemostasis and thrombosis under arterial shear conditions.

What is your career goal and what are you doing next?

Right now, I am pursuing potential postdoc positions in the triangle area as I will be staying here for the next few years. What I plan on doing after that is still uncertain.

What was your research hypothesis or goal?

he overall goal of my research was to better understand the spatial and temporal dynamics of senescence induction. More specifically, how senescence emerges following DNA damage to healthy cells across long periods of time, how senescent cells influence their healthy neighbors through secreted factors, and how the burden of senescent cells accumulates in an age-related disease such as osteoarthritis.

What were the major findings from your PhD research?

I found that there is significant heterogeneity in how senescence arises from healthy cells. Only a small fraction of all senescent cells express the factors which negatively influence their healthy neighbors. Additionally, there is an increased senescence burden in female synovial fibroblasts in osteoarthritis. This increased senescence burden could help explain why females are more likely to develop OA.

What is your career goal and what are you doing next?

I want to stay in academia and run my own lab, here at UNC if it works out that way! My next step on the path to that goal will be a postdoc with Mohanish Deshmukh studying cellular senescence in the brain!