Rafal Pawlinski
University of North Carolina at Chapel Hill, NC·Medicine & Clinical Research
Sickle cell disease (SCD) is an inherited blood disorder caused by a single-letter change in the β-globin gene, which encodes part of hemoglobin. When oxygen is low, red blood cells bend into a sickle shape.
- Fields
Medicine & Clinical Research
Physiology
Biochemistry
- Topics
sickle cell disease
Factor XII
FXIIa
- Grants
- 1 known grant, through Jun 2028
What they work on
- Identify the disease-specific triggers that activate Factor XII, a protein that starts blood clotting, in sickle cell disease, using blood samples from patients and a mouse model of the disease.
- Characterize how Factor XII changes the behavior of neutrophils, inflammatory white blood cells, including their activation and adhesion, in sickle cell disease.
- Compare the inactive precursor (zymogen) and active enzyme (FXIIa) forms of Factor XII, and FXII made by different cell types, in vessel blockage and vein clotting, using pharmacologic and genetic tools in SCD mice.
- Determine whether long-term Factor XII deficiency slows disease progression and reduces early mortality in a mouse model of sickle cell disease.
More about the research
This causes painful blockages of small blood vessels, called vaso-occlusive crises (VOC), as well as anemia from red cells bursting and, over time, damage to many organs. Patients also have blood that clots too easily, which raises their risk of venous thrombosis (VT), clots that form in veins. Newer blood thinners still increase bleeding. This project asks whether Factor XII (FXII), a blood protein that can start the clotting process, drives these complications in ways that could be blocked more safely.
Why it matters
Deep vein thrombosis and vaso-occlusive crises cause severe pain, organ damage and early death in people with sickle cell disease. Current anticoagulants carry a bleeding risk. By showing how Factor XII drives clotting and blood-vessel blockage, this work could support therapies that inhibit FXII. Such drugs may prevent clots and ease vaso-occlusive crises without causing bleeding.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Enrico Novelli
University of Pittsburgh, PA·Medicine & Clinical Research
Determine whether hemin, a toxic breakdown product of hemoglobin, and hypoxia (low oxygen) trigger VLA-4-driven blood-cell stickiness in sickle cell mice, measured by PET imaging with the tracer 64Cu-LLP2A.
Yohei Hisada
University of North Carolina at Chapel Hill, NC·Medicine & Clinical Research
Test whether podoplanin on leukemia blast cells drives platelet loss in acute promyelocytic leukemia by activating platelets through their CLEC-2 receptor, using xenograft and allograft mouse models that reproduce patient clotting abnormalities.
Renee Manworren
University of Texas at Arlington, TX·Medicine & Clinical Research
Collect pain-related gene variants, NIH HEAL common data elements, social determinants of health and other biopsychosocial data over time from 1,000 Black adolescents and young adults with sickle cell disease in three U.S. regions.
The school
University of North Carolina at Chapel Hill: 72 labs on PI Pages, $1.6B a year on research, 523 research doctorates a year.
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