Role of Satellite Cell Secreted Vascular Endothelial Growth Factor in Promoting Angiogenesis Restricted; Files Only
Ren, Tianjiao (Spring 2022)
Published
Abstract
Peripheral Artery Disease (PAD) is prevalent in the United States. The estimated lifetime risk of PAD in 2021 was estimated to be 19%, 22%, and 30% in White, Hispanic, and Black Americans, respectively (1). Symptoms include difficulty walking and claudication. Prolonged and untreated PAD can progress to critical limb ischemia (2). Patients may be candidates for angioplasty to reopen arteries or bypass surgery to revascularize around the affected area (3) (4) (5). Current non-invasive treatment to promote revascularization via exercise therapy is insufficient, as individual response varies. Satellite cells (SCs) are muscle progenitor cells localized near capillaries beneath the basal lamina of muscle fibers. SCs play a role in skeletal muscle repair and adaptation to exercise (6). In addition to their role in myofiber differentiation, SCs also play a role in promoting angiogenesis tube formation and increasing vascular flow (7). The mechanism of this is largely unknown. Previous studies have shown increased and similar angiogenesis in response to conditioned media from SCs and SC co-culture, suggesting paracrine signaling (8). Preliminary data has shown that encapsulated SCs delivered near the ischemic injury site significantly improve vascular growth and perfusion in hind limb ischemic mouse models (9). In the literature, vascular endothelial growth factor (VEGF) is commonly believed to be the key factor responsible for this angiogenesis (10) (11). However, there may be additional factors that play a role in SC promoted collateral vessel growth. SCs with the receptor for advanced glycation end products (RAGE) knocked out had equal expression of VEGF as wildtype SCs, but only the wildtype cells improved vascular response (9). This led to the hypothesis that VEGF is not the only paracrine factor responsible for inducing angiogenesis. To study the role of SC secreted VEGF on angiogenesis, VEGF expression was knocked down in SCs using siRNA silencer. Migration assays using mouse aortic smooth muscle cells (MASMs) and human aortic endothelial cells (HAECs) allowed for isolated study of the effect of VEGF knockdown SCs on smooth muscle and endothelial cell migration. MASMs showed no significant differential migration towards the stimulus of VEGF knockdown SCs versus control SCs, suggesting additional SC secreted factors promote smooth muscle cell chemotaxis.
Table of Contents
Introduction................................................................................................................................... 1 Methods.......................................................................................................................................... 4
Results ............................................................................................................................................ 7 Discussion..................................................................................................................................... 10
Supplemental Material ............................................................................................................... 12
References .................................................................................................................................... 14
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File download under embargo until 27 May 2024 | 2022-05-03 21:11:20 -0400 | File download under embargo until 27 May 2024 |
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