Loss of Spry1 in vascular smooth muscle cells promotes hypercholesterolemiainduced VSMC phenotypic transitions and regulates atherogenesis

Authors

Xuehui Yang, Maine Medical Center
Shivangi Pande, Maine Medical Center
Robert Friesel, Maine Medical Center

Document Type

Poster

Publication Date

4-30-2020

Institution/Department

Maine Medical Center, Medical Education, Maine Medical Center Research Institute, Center for Molecular Medicine

MeSH Headings

Muscle, Smooth, Vascular, Myocytes, Smooth Muscle, Atherosclerosis

Abstract

Atherosclerosis is an inflammatory disease characterized by arterial wall thickening and plaque accumulation, and is a major cause of death worldwide. Vascular smooth muscle cells (VSMC), which have the unique ability to transition from mature contractile cells to myofibroblasts and macrophagelike foam cells, and adopt a proinflammatory state contribute to atherogenic microenvironment (1). We aimed to investigate how Spry1, a regulator of receptor tyrosine kinase signaling, affects hypercholesterolemia induced plaque formation in mice by manipulating Spry1 expression specifically in VSMC.

Comments

2020 Costas T. Lambrew Research Retreat

Recommended Citation

Yang, Xuehui; Pande, Shivangi; and Friesel, Robert, "Loss of Spry1 in vascular smooth muscle cells promotes hypercholesterolemiainduced VSMC phenotypic transitions and regulates atherogenesis" (2020). Costas T. Lambrew Research Retreat 2020. 17.
https://knowledgeconnection.mainehealth.org/lambrew-retreat-2020/17