Cardiovascular disease remains the number one cause of mortality in humans. Using mouse models of genetic disruption, I have previously found that Bmal1 has an important vascular-specific role controlling hypermuscularization and scarring in the blood vessel in a process called pathological remodeling or stiffening. I have also found that the endothelial cell layer of arteries contributes to the disease in Bmal1 knockout (KO) mice. While Bmal1 is found throughout the body, its functional though much less understood paralog, Bmal2, is more selectively expressed in the endothelium. To understand the role of Bmal2 in vascular disease, I have implemented a widely used experimental animal model of arterial ligation to induce vascular remodeling. I ligated the left common carotid artery (LC) in two groups of mice, control wild-type mice (no genetic mutation) and the experimental Bmal2-KO (global knockout) mice. After two weeks, I isolated the LC and fixed the arteries in optimal cutting temperature (O.C.T.) compound and conducted histological processing (cut cross sections with a cryotome and stained with hematoxylin and eosin). I then quantified the changes in structure in the artery using the ImageJ program on digitized microscope images. My preliminary results suggest that compared to control mice, thickening of the LC was observed in female Bmal2-KO mice only and not in the male Bmal2-KO mice, indicating Bmal2 may have a sex-specific role in vascular remodeling. Future studies will assess the endothelial specific knockout mouse of Bmal2.


We would like to thank the Department of Pharmacology and Toxicology, amd the Chair, Dr. Alvin Terry, and the National Institutes of Health and Aging for providing this project.

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