Paper - WANFANG MED ONLINE

You Position: Home > Paper

MicroRNA alterations in senescent endothelial progenitor cells induced by remnant-like lipoproteins

( views:138, downloads:8 )

Author:: No author available

Journal Title:: Chinese Medical Journal

Issue:: 19

DOI:: 10.3760/cma.j.issn.0366-6999.2012.19.021

Key Word:: remnant-like lipoproteins;endothelial progenitor cells;senescence;microRNAs

Abstract： Background Remnant-like lipoproteins (RLPs) have been demonstrated to accelerate the onset of endothelial progenitor cells (EPCs) senescence.Recent study has determined that microRNAs (miRNAs) were closely associated with cellular proliferation and senescence.This study aimed to examine whether RLPs lead to an alteration of miRNAs in senescent EPCs.Methods RLPs were prepared from plasma samples with immunoaffinity method.After 8 days of culture,EPCs were identified by flow cytometry analysis.Cells were incubated with RLPs for 72 hours.The senescent markers p16INK4a and senescence-associated beta-galactosidase (SA-β-gal) were detected by Western blotting analysis and β-gal staining assay,respectively.A human miRNA microarray containing 723 miRNAs was used to detect the expression profile of miRNAs in control and senescent EPCs.The result from the above microarray was qualified by RT-PCR assay.Results RLPs dose-dependently up-regulated the protein level of p1 6INK4a in EPCs,and RLPs at a concentration of 100μg/ml induced a significant increase in the percentage of SA-β-gal-positive EPCs.Of 723 miRNAs,four miRNAs expressed differentially and significantly in RLPs-treated EPCs (P ＜0.05),then their changes in expression were validated by real-time RT-PCR.Among them miR-148b and miR-155 were upregulated while miR-574-3p was down-regulated significantly when compared with control (P ＜0.01).Conclusions RLPs result in the onset of EPCs senescence.Senescent EPCs induced by RLPs exhibit a different profile of miRNAs.These three miR-148b and miR-155 and miR-574-3p reach a significant difference when compared with control,indicating that microRNA might take part in RLPs-induced EPCs senescence.Chin Med J 2012;125(19):3479-3484

Reference

[1]Cho,H.H.,Kim,Y.J.,Lee,S.Y.,etc.Mir-486-5p induces replicative senescence of human adipose tissue-derived mesenchymal stem cells and its expression is controlled by high glucose[J].2012,21(10).
[2]Yeligar S,Tsukamoto H,Kalra VK.Ethanol-induced expression of ET-1 and ET-BR in liver sinusoidal endothelial cells and human endothelial cells involves hypoxia-inducible factor-1alpha and microrNA-199.[J].2009,183(8).
[3]Liu L,Zheng XY,Yang DG.Cyclin-dependent kinase inhibitor p16(INK4a) and telomerase may co-modulate endothelial progenitor cells senescence.[J].2008,7(2).
[4]Bernard S, Marasa,Subramanya, Srikantan,Jennifer L, Martindale,etc.MicroRNA profiling in human diploid fibroblasts uncovers miR-519 role in replicative senescence.[J].2010,2.
[5]Seals,D.R.,Lawson,B.R.,Magerko,K.A.,etc.MicroRNA changes in human arterial endothelial cells with senescence: Relation to apoptosis, eNOS and inflammation[J].2012,47(1).
[6]Yu W,Han N,Liu Y,etc.Profiles of oxidative stress-related microRNA and mRNA expression in auditory cells.[J].2010,1346.
[7]Liu L,Wen T,Zheng XY,etc.Remnant-like particles accelerate endothelial progenitor cells senescence and induce cellular dysfunction via an oxidative mechanism.[J].2009,202(2).
[8]Hideki Doi,Kiyotaka Kugiyama,Hideki Oka,etc.Remnant Lipoproteins Induce Proatherothrombogenic Molecules in Endothelial Cells Through a Redox-Sensitive Mechanism[J].2000,102(6).
[9]Kim I,Morrison SJ,Chada K,etc.Hmga2 Promotes Neural Stem Cell Self-Renewal in Young but Not Old Mice by Reducing p16(Ink4a) and p19(Arf) Expression[J].2008,135(2).
[10]Taniyama,Y.,Chatterjee,A.,Morishita,R.,etc.Inhibition of Lp(a)-induced functional impairment of endothelial cells and endothelial progenitor cells by hepatocyte growth factor[J].2012,423(1).
[11]K, Kugiyama,H, Doi,K, Takazoe,etc.Remnant lipoprotein levels in fasting serum predict coronary events in patients with coronary artery disease.[J].1999,99.
[12]H N, Hodis.Triglyceride-rich lipoprotein remnant particles and risk of atherosclerosis.[J].1999,99.
[13]Freund A,Orjalo AV,Desprez PY,etc.Inflammatory networks during cellular senescence: causes and consequences.[J].2010,16(5).
[14]Qiu,Li G,Luna C.Alterations in microRNA expression in stress-induced cellular senescence.[J].2009,130(11).
[15]Frenquelli M,Scielzo C,Rossi C,etc.MicroRNA and proliferation control in chronic lymphocytic leukemia: functional relationship between miR-221/222 cluster and p27.[J].2010,115(19).
[16]Akasaka T,Obana M,Kuki S,etc.Hyperglycemia accelerated endothelial progenitor cell senescence via the activation of p38 mitogen-activated protein kinase.[J].2006,70(8).
[17]Kuehbacher A,Urbich C,Dimmeler S.Role of microRNAs in vascular diseases, inflammation, and angiogenesis.[J].2008,79(4).
[18]Subramanian, Murugan,Yaniv, Yael,Yang, Xiaoling,etc.Growth Inhibition by miR-519 via Multiple p21-Inducing Pathways[J].2012,32(13).
[19]Tabuchi T,Itoh T,Nakamura M,etc.Effect of atorvastatin on microRNA 221/222 expression in endothelial progenitor cells obtained from patients with coronary artery disease.[J].2009,39(5).
[20]Masuda H,Asahara T,Kearney M,etc.Transplantation of ex vivo expanded endothelial progenitor cells for therapeutic neovascularization.[J].2000,97(7).
[21]Zhao T,Li J,Chen AF.MicroRNA-34a induces endothelial progenitor cell senescence and impedes its angiogenesis via suppressing silent information regulator 1.[J].2010,299(1 Pt.1).
[22]Chotani M,Jiang J,Nuovo GJ,etc.The human angiotensin II type 1 receptor +1166 A/C polymorphism attenuates microrna-155 binding.[J].2007,282(33).
[23]B, van der Loo,M J, Fenton,J D, Erusalimsky.Cytochemical detection of a senescence-associated beta-galactosidase in endothelial and smooth muscle cells from human and rabbit blood vessels.[J].1998,241.