Bio

I received my B.S. in Microbiology, and M.S. in Cell and Molecular Biology from San Francisco State University. Currently, I am a Biology Ph.D. student with an emphasis in Cell, Molecular and Organismal Biology at Stanford University. I am interested in a range of topics, from cell biology to cancer immunology, however, my research interests lie primarily in understanding the cellular mechanisms at play in genetic and autoimmune diseases.

Institute Affiliations

Education & Certifications

  • M.S., San Francisco State University, Cell and Molecular Biology (2018)
  • B.S., San Francisco State University, Microbiology (2016)

Contact

Additional Info

  • Mail Code: 5020

All Publications

  • Endocardium-to-coronary artery differentiation during heart development and regeneration involves sequential roles of Bmp2 and Cxcl12/Cxcr4. Developmental cell D'Amato, G., Phansalkar, R., Naftaly, J. A., Fan, X., Amir, Z. A., Rios Coronado, P. E., Cowley, D. O., Quinn, K. E., Sharma, B., Caron, K. M., Vigilante, A., Red-Horse, K. 2022

    Abstract

    Endocardial cells lining the heart lumen are coronary vessel progenitors during embryogenesis. Re-igniting this developmental process in adults could regenerate blood vessels lost during cardiac injury, but this requires additional knowledge of molecular mechanisms. Here, we use mouse genetics and scRNA-seq to identify regulators of endocardial angiogenesis and precisely assess the role of CXCL12/CXCR4 signaling. Time-specific lineage tracing demonstrated that endocardial cells differentiated into coronary endothelial cells primarily at mid-gestation. A new mouse line reporting CXCR4 activity-along with cell-specific gene deletions-demonstrated it was specifically required for artery morphogenesis rather than angiogenesis. Integrating scRNA-seq data of endocardial-derived coronary vessels from mid- and late-gestation identified a Bmp2-expressing transitioning population specific to mid-gestation. Bmp2 stimulated endocardial angiogenesis in vitro and in injured neonatal mouse hearts. Our data demonstrate how understanding the molecular mechanisms underlying endocardial angiogenesis can identify new potential therapeutic targets promoting revascularization of the injured heart.

    View details for DOI 10.1016/j.devcel.2022.10.007

    View details for PubMedID 36347256

  • Blood flow modeling reveals improved collateral artery performance during the regenerative period in mammalian hearts. Nature cardiovascular research Anbazhakan, S., Rios Coronado, P. E., Sy-Quia, A. N., Seow, L. W., Hands, A. M., Zhao, M., Dong, M. L., Pfaller, M. R., Amir, Z. A., Raftrey, B. C., Cook, C. K., D'Amato, G., Fan, X., Williams, I. M., Jha, S. K., Bernstein, D., Nieman, K., Pașca, A. M., Marsden, A. L., Horse, K. R. 2022; 1 (8): 775-790

    Abstract

    Collateral arteries bridge opposing artery branches, forming a natural bypass that can deliver blood flow downstream of an occlusion. Inducing coronary collateral arteries could treat cardiac ischemia, but more knowledge on their developmental mechanisms and functional capabilities is required. Here we used whole-organ imaging and three-dimensional computational fluid dynamics modeling to define spatial architecture and predict blood flow through collaterals in neonate and adult mouse hearts. Neonate collaterals were more numerous, larger in diameter and more effective at restoring blood flow. Decreased blood flow restoration in adults arose because during postnatal growth coronary arteries expanded by adding branches rather than increasing diameters, altering pressure distributions. In humans, adult hearts with total coronary occlusions averaged 2 large collaterals, with predicted moderate function, while normal fetal hearts showed over 40 collaterals, likely too small to be functionally relevant. Thus, we quantify the functional impact of collateral arteries during heart regeneration and repair-a critical step toward realizing their therapeutic potential.

    View details for DOI 10.1038/s44161-022-00114-9

    View details for PubMedID 37305211

    View details for PubMedCentralID PMC10256232