title: Schlafen 1 inhibits the proliferation and tube formation of endothelial progenitor cells.
abstract: Endothelial progenitor cells (EPCs) are the major source of cells that restore the endothelium during reendothelialization. This study was designed to investigate whether Schlafen 1 (Slfn1) has an effect on the proliferation and tube formation of EPCs in vivo. Slfn1 was expressed in rat EPCs. The overexpression of Slfn1 suppressed the proliferation and tube formation of EPCs; conversely, the knockdown of Slfn1 by shRNA promoted the proliferation and tube formation of EPCs. Furthermore, when Slfn1 was overexpressed, the EPCs were arrested in the G1 phase of the cell cycle. In contrast, when Slfn1 was knocked down, the EPCs progressed into the S phase of the cell cycle. Additionally, the overexpression of Slfn1 decreased the expression of Cyclin D1, whereas the knockdown of Slfn1 increased the expression of Cyclin D1; these findings suggest that Cyclin D1 is downstream of Slfn1 in Slfn1-mediated EPC proliferation. Taken together, these results indicate a key role for Slfn1 in the regulation of EPC biological behavior, which may provide a new target for the use of EPCs during reendothelialization.
authors.affiliation: Department of Cardiovascular Diseases, The People's Hospital of Guizhou Province, Nanming District, Guiyang, People's Republic of China.
authors.forename: Chun-yan
authors.initials: CY
authors.lastname: Kuang
authors.affiliation: Department of Cardiovascular Diseases, The People's Hospital of Guizhou Province, Nanming District, Guiyang, People's Republic of China.
authors.forename: Tian-he
authors.initials: TH
authors.lastname: Yang
authors.affiliation: Department of Cardiovascular Diseases, The People's Hospital of Guizhou Province, Nanming District, Guiyang, People's Republic of China.
authors.forename: Yang
authors.initials: Y
authors.lastname: Zhang
authors.affiliation: Medical examination center, The People's Hospital of Guizhou Province, Nanming District, Guiyang, People's Republic of China.
authors.forename: Lu
authors.initials: L
authors.lastname: Zhang
authors.affiliation: Department of Cardiovascular Diseases, The People's Hospital of Guizhou Province, Nanming District, Guiyang, People's Republic of China.
authors.forename: Qiang
authors.initials: Q
authors.lastname: Wu
mesh_terms: D000818:Animals; D001854:Bone Marrow Cells / Q000166:cytology; D018797:Cell Cycle Proteins / Q000172:deficiency / Q000235:genetics / Q000378:metabolism*; D049109:Cell Proliferation; D066026:Endothelial Progenitor Cells / Q000166:cytology*; D020868:Gene Silencing; D042541:Intracellular Space / Q000378:metabolism; D008297:Male; D021381:Protein Transport; D034741:RNA, Small Interfering / Q000235:genetics; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D018797:Cell Cycle Proteins; D034741:RNA, Small Interfering; C000598725:Slfnl1 protein, rat