title: The effect of endothelial progenitor cells on angiotensin II-induced proliferation of cultured rat vascular smooth muscle cells.
abstract: Previous studies have demonstrated that endothelial progenitor cells (EPCs) could delay the progress of vascular remodeling in blood vessel-proliferating diseases. The proliferation of vascular smooth muscle cells (VSMCs) is a pivotal factor in cardiovascular diseases. In this study, we investigated whether EPCs could inhibit the Angiotensin II (Ang II)-induced proliferation of VSMCs. The effect of early EPC-conditioned medium (E-EPC-CM), late EPCs-CM (L-EPC-CM), and HUVEC-CM on Ang II-induced proliferation of VSMCs was assessed by BrdU incorporation, total protein content, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assays, and flow cytometry. Reverse transcriptase-polymerase chain reaction and Western blot were performed to analyze the effect of different CMs on Ang II-induced phosphorylations of ERK, JNK, p38, and NF-κB subunit p65 and the expressions of c-myc and c-fos. E-EPC-CM, L-EPC-CM, and HUVEC-CM significantly inhibited the Ang II-induced DNA synthesis, total protein expression, cell survival, and cell cycle progress of VSMCs. Furthermore, E-EPC-CM significantly inhibited the Ang II-induced phosphorylation of ERK, JNK, p38, and p65 (nuclear translocation of p65) and the expressions of c-myc and c-fos. Taken together, these data suggested that EPCs may delay the progress of vascular remodeling in blood vessel-proliferating diseases by inhibiting Ang II-induced proliferation of VSMCs through inactivating MAPKs and NF-κB signaling pathways and by reducing the expressions of c-myc and c-fos.
authors.affiliation: Department of Geriatric Cardiology, Xiangya Hospital, Changsha, China.
authors.forename: Li
authors.initials: L
authors.lastname: Fang
authors.forename: Mei-Fang
authors.initials: MF
authors.lastname: Chen
authors.forename: Zhi-Lin
authors.initials: ZL
authors.lastname: Xiao
authors.forename: Guo-Long
authors.initials: GL
authors.lastname: Yu
authors.forename: Xiao-Bin
authors.initials: XB
authors.lastname: Chen
authors.forename: Xiu-Mei
authors.initials: XM
authors.lastname: Xie
mesh_terms: D000804:Angiotensin II / Q000494:pharmacology*; D000818:Animals; D015153:Blotting, Western; D049109:Cell Proliferation / Q000187:drug effects*; D002478:Cells, Cultured; D004730:Endothelium, Vascular / Q000166:cytology / Q000378:metabolism; D005434:Flow Cytometry; D061307:Human Umbilical Vein Endothelial Cells; D006801:Humans; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism; D009131:Muscle, Smooth, Vascular / Q000166:cytology / Q000187:drug effects; D032389:Myocytes, Smooth Muscle / Q000187:drug effects* / Q000378:metabolism; D016328:NF-kappa B / Q000378:metabolism; D010766:Phosphorylation / Q000187:drug effects; D051381:Rats; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015398:Signal Transduction; D013234:Stem Cells / Q000378:metabolism*
chemical_list: D016328:NF-kappa B; D000804:Angiotensin II; D020928:Mitogen-Activated Protein Kinases