header-logo
Research Group Lab Hall
Magdalena Chrzanowska, PhD, FAHA

Magdalena Chrzanowska, PhD, FAHA

Associate Professor, Pharmacology and Toxicology; Program Leader, Transfusion Medicine, Vascular Biology and Cell Therapy and Senior Investigator; Versiti Blood Research Institute

Locations

  • Versiti Blood Center of Wisconsin

Education

PhD, Cell and Cardiovascular Biology, University of North Carolina at Chapel Hill, 1997

Research Interests

At the Vascular Signaling Lab, we are dedicated to understanding the multifaceted role of endothelial cells in health and disease. Led by Dr. Magdalena Chrzanowska, our work is anchored in elucidating the function of a small GTPase Rap1 in the endothelium.

We have uncovered pivotal roles of Rap1 isoforms—Rap1A and Rap1B—in the endothelium, influencing critical aspects of endothelial function, including nitric oxide release, VEGFR2 signaling, angiogenesis and dynamic regulation of vascular permeability. Specifically, Rap1B plays a key role in mitigating inflammatory responses and influencing tumor progression.

Our current endeavors are directed at unraveling the physiological and pathological consequences of endothelial cell (EC) Rap1 activity and unraveling the cellular mechanisms of Rap1.

Ongoing projects:

  1. Endothelial control of heart function R01HL157893
    Understanding how ECs communicate with cardiac myocytes is critical for the regulation of cardiac contractile function. We are investigating how Rap1 isoforms in coronary (vascular) and heart microcapillary (cardiac) endothelial compartments control endothelial-smooth muscle cells and endothelial-cardiac myocyte communication to maintain coronary vessel function and cardiac contractility.

  2. Endothelial Rap1 in ischemic retinopathy R01EY036588 start 7/1/24
    With diabetic retinopathy the most common microvascular complication and the leading cause of acquired vision loss worldwide, our focus is the Rap1-driven mechanisms that control endothelial-leukocyte interactions, aiming to alleviate the inflammatory responses that contribute to retinal damage.

  3. EC mechanisms controlling hematopoiesis
    The bone marrow's vascular niche is essential for hematopoietic stem cell regulation and its disruption is linked with blood disorders. We are examining the mechanisms through which Rap1 in bone marrow ECs impacts hematopoiesis and erythropoiesis.

  4. EC Rap1 in tumor microenvironment
    Our research addresses the critical challenge of immunosuppression within tumor vasculature, crucial for advancing cancer immunotherapy. We've identified that endothelial Rap1B inhibits T-cell activity, promoting tumor growth. Currently, we are probing the mechanisms through which endothelial Rap1 modulates VEGF-driven immunosuppression and the interactions between tumor endothelial cells and leukocytes.

  5. Cell biology of Rap1A and Rap1B
    Our research is focused on dissecting the distinct and shared roles of Rap1A and Rap1B in endothelial functions. We investigate how Rap1A contributes to lung permeability and how Rap1B regulates the balance between endothelial homeostasis and inflammatory response, crucial for vascular health.

Our lab is committed to advancing understanding in these areas, striving for breakthroughs that can lead to innovative treatments for cardiovascular, ocular, hematopoietic, and cancer-related conditions.

Funding:
Current: R01HL157893 |  Endothelial Rap1 in the control of heart function
Pending: R01EY036588 |  Endothelial Rap1 restricts inflammation in the retina

Publications