Adventitial SCA-1+ progenitor cell gene sequencing reveals the mechanisms of cell migration in response to hyperlipidemia

Kokkinopoulos, Ioannis, Wong, Mei Mei, Potter, Claire M. F., Xie, Yao, Yu, Baoqi, Warren, Derek T., Nowak, Witold N., Le Bras, Alexandra, Ni, Zhichao, Zhou, Chao, Ruan, Xiongzhong, Karamariti, Eirini, Hu, Yanhua, Zhang, Li and Xu, Qingbo (2017) Adventitial SCA-1+ progenitor cell gene sequencing reveals the mechanisms of cell migration in response to hyperlipidemia. Stem Cell Reports, 9 (2). 681–696.

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Adventitial progenitor cells, including SCA-1+ and mesenchymal stem cells, are believed to be important in vascular remodeling. It has been shown that SCA-1+ progenitor cells are involved in neointimal hyperplasia of vein grafts, but little is known concerning their involvement in hyperlipidemia-induced atherosclerosis. We employed single-cell sequencing technology on primary adventitial mouse SCA-1+ cells from wild-type and atherosclerotic-prone (ApoE-deficient) mice and found that a group of genes controlling cell migration and matrix protein degradation was highly altered. Adventitial progenitors from ApoE-deficient mice displayed an augmented migratory potential both in vitro and in vivo. This increased migratory ability was mimicked by lipid loading to SCA-1+ cells. Furthermore, we show that lipid loading increased miRNA-29b expression and induced sirtuin-1 and matrix metalloproteinase-9 levels to promote cell migration. These results provide direct evidence that blood cholesterol levels influence vascular progenitor cell function, which could be a potential target cell for treatment of vascular disease.

Item Type: Article
Uncontrolled Keywords: vascular progenitors,adventitial migration,hyperlipidemia,atherosclerosis,extracellular matrix
Faculty \ School: Faculty of Science > School of Pharmacy
UEA Research Groups: Faculty of Science > Research Groups > Molecular and Tissue Pharmacology
Depositing User: Pure Connector
Date Deposited: 16 Sep 2017 05:06
Last Modified: 21 Oct 2022 16:31
DOI: 10.1016/j.stemcr.2017.06.011


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