Immunization of Arthritis Prone Mice with Malondialdehyde-Acetaldehyde (MAA) Modified Vimentin Induces Fibrotic Lung Changes

Poster presenter: Wenxian Zhou, BS, Medical Scientist Training Program Student, University of Nebraska Medical Center

Poster title: Immunization of Arthritis Prone Mice with Malondialdehyde-Acetaldehyde (MAA) Modified Vimentin Induces Fibrotic Lung Changes

Poster session B: Sunday, Nov. 17

What is your poster about?

“Our lab uncovered new insights into how lung fibrosis is promoted in an arthritis-prone mouse model. We found that immunizing arthritis-prone mice with malondialdehyde-acetaldehyde (MAA)-modified vimentin directly increased 1) MAA, citrulline (CIT), and vimentin deposition in lung tissue, 2) alveolar macrophage infiltration, and 3) fibrotic lung changes.”

Why did you decide to investigate this topic?

“Rheumatoid arthritis-associated interstitial lung disease (RA-ILD) is one of the leading causes of morbidity and mortality in RA patients. Our lab previously demonstrated increased circulating concentrations of anti-MAA antibodies and increased expression of MAA antigens in the lung tissues of RA-ILD patients. This study aims to explore whether MAA plays a pathogenic role in the development of RA-ILD.”

What are you working on next related to this research?

“Given that our data has shown that MAA and CIT modifications are overrepresented in RA and act together in promoting tissue fibrosis in lung tissues, we have initiated studies to explore whether these post-translational modifications might also impact extracellular matrix deposition and function in other tissues. My main project investigates how RA patients develop heart fibrosis, which leads to heart failure with preserved ejection fraction (HFpEF). I am currently studying how MAA and CIT trigger cellular activation and communication between human cardiac cell types, exacerbating cardiac inflammation and fibrosis. Additionally, I am testing whether MAA and CIT inhibitors can prevent the development of heart failure in collagen-induced arthritis mice.”

What excites you most about your work?

“Studying the underlying mechanisms driving RA complications is both intellectually intriguing and potentially clinically impactful. I am excited to discover new insights into how immune cells and resident cells interact with each other, change phenotypes, and drive disease progression. Moreover, knowing that my research might pave the way for better diagnostic and therapeutic options for RA patients inspires me to pursue this career. In addition, the supportive and collaborative training environment provided by my mentors and lab members makes conducting research highly enjoyable.”

What are you most looking forward to at ACR Convergence 2024 in Washington, D.C.?

“I am excited to learn about cutting-edge research in rheumatic diseases from experts in the field, network with other scientists, explore the city, and present my research to receive valuable feedback.”