Vasculopathy in COVID-19 and Pathogenesis of Cutaneous Vascular Malformations
Abstract
SARS-CoV-2-associated vasculopathy under hyperlipidemia and pathological progression of congenital vascular
abnormalities in Port Wine Stains. In the first part, we will present our clinical data for the first discovery of dyslipidemia
in COVID-19 patients which have been substantially recognized. Mechanistically, we have shown evidence of niche why
obese subjects are more vulnerable to SARS-CoV-2 attack. Using a spike protein–pseudotyped (Spp) lentivirus with the
proper tropism of the SARS-CoV-2 spike protein on the surface, we have found that Spp lentiviruses preferably attack to
endothelial cells in heart in obese but not normal weight mice, leading to exaggerated vasculopathy and cardiomyopathy.
Cells with over-expression of Spike protein have impaired lipid metabolic and autophagy formation pathways, resulting in
increased cell death in response to lipotoxicity. In the second part, we will discuss the clinical molecular pathology of
infantile and early childhood PWS to show that (1) PWS is a disease with pathological alterations involving the entire skin
physiological milieu; (2) pluripotent cells with the GNAQ (R183Q) may give rise to multilineages in PWS; and (3) exocytosis
of extracellular vesicles is enhanced in PWS vasculatures.
Biography
Dr. Tan received his medical degree and master degree in Molecular Biology from XiangYa School of Medicine, China. He
received his PhD in neurobiology and neurophysiology from University of California, Los Angeles. He joined Beckman
Laser Institute at UC Irvine as an assistant project scientist in 2010 under the mentorship of Dr. Stuart Nelson. In 2018,
he joined the department of cell biology and anatomy at School of Medicine University of South Carolina as an associate
professor.
Sponsored by the Michael and Roberta Berns Laser Microbeam Program
