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• W2067129712 abstract "HomeCirculation ResearchVol. 104, No. 9Vascular Progenitor Cells in Diabetes Mellitus Free AccessEditorialPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessEditorialPDF/EPUBVascular Progenitor Cells in Diabetes MellitusRoles of Wnt Signaling and Negatively Charged Low-Density Lipoprotein Chu-Huang Chen, Richard A.F. Dixon, Liang-Yin Ke and James T. Willerson Chu-Huang ChenChu-Huang Chen From the Department of Medicine, Baylor College of Medicine (C.-H.C., L.-Y.K.), Houston, Tex; Texas Heart Institute (R.A.F.D., J.T.W.), Houston; China Medical University Hospital (C.-H.C.), Taichung, Taiwan; and Kaohsiung Medical University Hospital (L.-Y.K.), Kaohsiung, Taiwan. Search for more papers by this author , Richard A.F. DixonRichard A.F. Dixon From the Department of Medicine, Baylor College of Medicine (C.-H.C., L.-Y.K.), Houston, Tex; Texas Heart Institute (R.A.F.D., J.T.W.), Houston; China Medical University Hospital (C.-H.C.), Taichung, Taiwan; and Kaohsiung Medical University Hospital (L.-Y.K.), Kaohsiung, Taiwan. Search for more papers by this author , Liang-Yin KeLiang-Yin Ke From the Department of Medicine, Baylor College of Medicine (C.-H.C., L.-Y.K.), Houston, Tex; Texas Heart Institute (R.A.F.D., J.T.W.), Houston; China Medical University Hospital (C.-H.C.), Taichung, Taiwan; and Kaohsiung Medical University Hospital (L.-Y.K.), Kaohsiung, Taiwan. Search for more papers by this author and James T. WillersonJames T. Willerson From the Department of Medicine, Baylor College of Medicine (C.-H.C., L.-Y.K.), Houston, Tex; Texas Heart Institute (R.A.F.D., J.T.W.), Houston; China Medical University Hospital (C.-H.C.), Taichung, Taiwan; and Kaohsiung Medical University Hospital (L.-Y.K.), Kaohsiung, Taiwan. Search for more papers by this author Originally published8 May 2009https://doi.org/10.1161/CIRCRESAHA.109.198051Circulation Research. 2009;104:1038–1040Over the centuries, diabetes mellitus–associated ischemic ulcers have driven physicians to continue to improve their skills in healing the ulcers to prevent devastating complications.1 Unfortunately, extremity amputation still remains the outcome in many cases. The recent development of vascular progenitor cell (PC) transplantation aimed at enhancing angiogenesis and wound healing may, however, provide new hope in the treatment of this old ailment.2,3 In this issue of Circulation Research, Barcelos et al show in a murine diabetes mellitus model that topical transplantation of human fetal CD133+ PCs significantly accelerates the healing of skin wounds on ischemic hind limbs.4 Their data suggest that the reparative angiogenesis is mediated by the wingless (Wnt) signaling pathway.The prominin-1 (PROM1)/CD133 gene encodes a pentaspan transmembrane glycoprotein expressed in a variety of stem cells, including hematopoietic stem cells, endothelial PCs (EPCs), and neuronal/glial stem cells.5,6 By suppressing further differentiation, PROM1 helps these cells maintain their stem cell properties. Mutations in PROM1 may result in retinitis pigmentosa,7 and its overexpression is also associated with cancer formation.8 In view of this cancer potential, overstimulation of CD133+ cells may also lead to unwanted consequences. Additionally, that human fetal CD133+ cells are not easily accessible makes this approach clinically impractical. Of importance, however, the gist of the work by Barcelos et al4 is not in promoting the use of human fetal CD133+ cells in common practice but, rather, in the enhancement of Wnt-dependent signaling in local endothelial cells (ECs) induced by PROM1/CD133 through a paracrine mechanism. This is supported by the success of CD133+ cell–conditioned medium (CCM) in producing CD133+-like effects. The capability of Wnt antagonists to prevent the CD133+ CCM effects suggests a mediator role for Wnt signaling. The observation by Barcelos et al is supported by another recent report in Circulation Research describing a Wnt-dependent mechanism of EC differentiation from embryonic stem cells.9By conveying information from the cell surface to the nucleus, the Wnt signaling pathway regulates embryonic development and cell fate decisions.10 On adhering to Frizzled (Fz) and low-density lipoprotein (LDL) receptor–related protein 5/6, Wnt ignites the canonical signaling pathway to deactivate the Axin/adenomatous polyposis coli/glycogen synthase kinase-3β complex. This acts to stabilize β-catenin by preventing its phosphorylation.11 Some β-catenin is then able to enter the nucleus and interact with the T-cell factor (TCF) family of transcription factors to promote specific gene expression. The β-catenin and TCF interaction can be inhibited by forkhead box transcription factor subgroup O (FOXO) proteins, which compete with TCF for β-catenin.12 Fortunately, the activity of both FOXO and glycogen synthase kinase-3β can be suppressed by phosphatidylinositol 3-kinase (PI3K)-Akt, another primary signaling pathway that may act synergistically with the Wnt canonical pathway. Here, the authors demonstrate that CD133+ PCs can secrete vascular endothelial growth factor (VEGF)-A, which activates PI3K-Akt through the kinase insert domain receptor (also known as VEGF receptor 2) to directly inhibit FOXO. Additionally, the CD133+ PC-released VEGF-A can stimulate local ECs to express Wnt proteins and ignite Wnt signaling (Figure). Download figureDownload PowerPointFigure. L5 counteracts CD133+-activated Wnt signaling in ECs or vascular PCs. Green arrow indicates stimulation; red line with end bar, inhibition; blue arrow, direction. APC, adenomatous polyposis coli; GSK, glycogen synthase kinase; KDR, kinase insert domain receptor; LRP, LDL receptor-related protein; LOX1, lectin-like oxidized LDL receptor-1.Although this approach may seem effective for stimulating angiogenesis, certain concerns remain. Besides VEGF-A, CD133+ PCs release broad-spectrum interleukins (ILs) and other chemokines, which may elicit nonspecific inflammatory reactions. Successful inhibition of the reactive angiogenesis by VEGF-A- and IL-8–neutralizing antibodies further indicates the inflammatory nature of the angiogenic response.13 VEGF- and IL-8–associated angiogenesis is also inducible by oxidized phospholipids, such as oxidized 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphorylcholine.14 VEGF-mediated angiogenesis often leads to the formation of premature capillaries with increased permeability.15 Furthermore, IL-8 activation may contribute to atherosclerotic advancement,16 worsening tissue perfusion. Fibroblast growth factor (FGF)2, whose participation in CD133+ cell–related Wnt signaling is not discussed in the present study, is more closely related to compensatory vasculogenesis.17 Because FGF2 and VEGF are both critical to tissue repair,13 it is important to examine how diabetes mellitus modulates angiogenic activities regulated by these growth factors.L5 is a highly negatively charged LDL circulating in patients with type 2 diabetes, with hypercholesterolemia, or who are smokers.18–21 In the absence of ex vivo oxidation, L5 induces EC apoptosis and inhibits EPC differentiation by disrupting FGF2 autoregulation via an FGF2-PI3K-Akt loop, mediated by the lectin-like oxidized LDL receptor-1.18–21 By inhibiting PI3K-Akt activation, L5 may offset the angiogenic effects of CD133+ PCs (Figure). In nondiabetic patients experiencing an acute myocardial infarction, there is often a surge of CD133+ PCs, such a compensatory response is dampened in those with-type 2 diabetes.22 Investigation of how L5 may contribute to PC insufficiency in diabetes is warranted. The mechanism of how L5 is produced in diabetes is still unclear but may involve adipocytic dysfunction. Wnt signaling also regulates adipocyte differentiation,23 although its role in diabetes development is still controversial.24Recent studies suggest that Wnt signaling is regulated by microRNAs (miRs), adding an additional level of complexity to this system. Expression of miR-8 potently antagonizes Wnt signaling, both by inhibiting Wnt-Fz interaction on the plasma membrane and by reducing TCF protein intracellularly.25 Additionally, miR-15a and miR-16-1 can also antagonize Wnt signaling, and reduction of these microRNAs promotes growth of prostate cancer cells.26 Thus, the role of Wnt signaling in EC or vascular PC activity is not totally clear at this time, and uncontrolled stimulation of this pathway may invite dangerous consequences. These considerations, including how L5 may counteract the CD133+ PC and Wnt interactions, are schematically summarized in the Figure.The opinions expressed in this editorial are not necessarily those of the editors or of the American Heart Association.We thank Suzanne Simpson for editorial assistance.Sources of FundingSupported by American Diabetes Association Research Grant 1-04-RA-13, a Pfizer Independent Research Grant, a Research Fund from Asia Chemical (Houston, Tex), and a Research Fund from Mao-Kuei Lin Foundation (Taiwan [to C.-H.C.]); and National Heart, Lung, and Blood Institute RFA grant HL-06-001 (Cardiovascular Cell Therapy Research Network, NIH [to J.T.W.]).DisclosuresNone.FootnotesCorrespondence to Chu-Huang Chen, MD, PhD, Baylor College of Medicine, 6565 Fannin St, MS A-601, Houston, TX 77030. E-mail [email protected] References 1 Cavanagh PR, Lipsky BA, Bradbury AW, Botek G. Treatment for diabetic foot ulcers. Lancet. 2005; 366: 1725–1735.CrossrefMedlineGoogle Scholar2 Friedrich EB, Walenta K, Scharlau J, Nickenig G, Werner N. CD34-/CD133+/VEGFR-2+ endothelial progenitor cell subpopulation with potent vasoregenerative capacities. Circ Res. 2006; 98: e20–25.LinkGoogle Scholar3 Rota M, LeCapitaine N, Hosoda T, Boni A, De Angelis A, Padin-Iruegas ME, Esposito G, Vitale S, Urbanek K, Casarsa C, Giorgio M, Luscher TF, Pelicci PG, Anversa P, Leri A, Kajstura J. Diabetes promotes cardiac stem cell aging and heart failure, which are prevented by deletion of the p66shc gene. Circ Res. 2006; 99: 42–52.LinkGoogle Scholar4 Barcelos LS, Duplaa C, Kränkel N, Graiani G, Invernici G, Katare R, Siragusa M, Meloni M, Campesi I, Monica M, Simm A, Campagnolo P, Mangialardi G, Stevanato L, Alessandri G, Emanueli C, Madeddu P. Human CD133+ progenitor cells promote the healing of diabetic ischemic ulcers by paracrine stimulation of angiogenesis and activation of Wnt signaling. Circ Res. 2009; 104: 1095–1102.LinkGoogle Scholar5 Yin AH, Miraglia S, Zanjani ED, Almeida-Porada G, Ogawa M, Leary AG, Olweus J, Kearney J, Buck DW. AC133, a novel marker for human hematopoietic stem and progenitor cells. Blood. 1997; 90: 5002–5012.CrossrefMedlineGoogle Scholar6 Griguer CE, Oliva CR, Gobin E, Marcorelles P, Benos DJ, Lancaster JR Jr, Gillespie GY. CD133 is a marker of bioenergetic stress in human glioma. PLoS ONE. 2008; 3: e3655.CrossrefMedlineGoogle Scholar7 Zhang Q, Zulfiqar F, Xiao X, Riazuddin SA, Ahmad Z, Caruso R, MacDonald I, Sieving P, Riazuddin S, Hejtmancik JF. Severe retinitis pigmentosa mapped to 4p15 and associated with a novel mutation in the PROM1 gene. Hum Genet. 2007; 122: 293–299.CrossrefMedlineGoogle Scholar8 Ricci-Vitiani L, Lombardi DG, Pilozzi E, Biffoni M, Todaro M, Peschle C, De Maria R. Identification and expansion of human colon-cancer-initiating cells. Nature. 2007; 445: 111–115.CrossrefMedlineGoogle Scholar9 Yang DH, Yoon JY, Lee SH, Bryja V, Andersson ER, Arenas E, Kwon YG, Choi KY. Wnt5a is required for endothelial differentiation of embryonic stem cells and vascularization via pathways involving both Wnt/β-catenin and protein kinase Cα. Circ Res. 2009; 104: 372–379.LinkGoogle Scholar10 Nusse R. Cell biology: relays at the membrane. Nature. 2005; 438: 747–749.CrossrefMedlineGoogle Scholar11 Tamai K, Semenov M, Kato Y, Spokony R, Liu C, Katsuyama Y, Hess F, Saint-Jeannet JP, He X. LDL-receptor-related proteins in Wnt signal transduction. Nature. 2000; 407: 530–535.CrossrefMedlineGoogle Scholar12 Jin T. The WNT signalling pathway and diabetes mellitus. Diabetologia. 2008; 51: 1771–1780.CrossrefMedlineGoogle Scholar13 Chen CH, Walterscheid JP. Plaque angiogenesis versus compensatory arteriogenesis in atherosclerosis. Circ Res. 2006; 99: 787–789.LinkGoogle Scholar14 Bochkov VN, Philippova M, Oskolkova O, Kadl A, Furnkranz A, Karabeg E, Afonyushkin T, Gruber F, Breuss J, Minchenko A, Mechtcheriakova D, Hohensinner P, Rychli K, Wojta J, Resink T, Erne P, Binder BR, Leitinger N. Oxidized phospholipids stimulate angiogenesis via autocrine mechanisms, implicating a novel role for lipid oxidation in the evolution of atherosclerotic lesions. Circ Res. 2006; 99: 900–908.LinkGoogle Scholar15 Witmer AN, Blaauwgeers HG, Weich HA, Alitalo K, Vrensen GF, Schlingemann RO. Altered expression patterns of VEGF receptors in human diabetic retina and in experimental VEGF-induced retinopathy in monkey. Invest Ophthalmol Vis Sci. 2002; 43: 849–857.MedlineGoogle Scholar16 Gharavi NM, Baker NA, Mouillesseaux KP, Yeung W, Honda HM, Hsieh X, Yeh M, Smart EJ, Berliner JA. Role of endothelial nitric oxide synthase in the regulation of SREBP activation by oxidized phospholipids. Circ Res. 2006; 98: 768–776.LinkGoogle Scholar17 Werner GS, Jandt E, Krack A, Schwarz G, Mutschke O, Kuethe F, Ferrari M, Figulla HR. Growth factors in the collateral circulation of chronic total coronary occlusions: relation to duration of occlusion and collateral function. Circulation. 2004; 110: 1940–1945.LinkGoogle Scholar18 Chen CH, Jiang T, Yang JH, Jiang W, Lu J, Marathe GK, Pownall HJ, Ballantyne CM, McIntyre TM, Henry PD, Yang CY. Low-density lipoprotein in hypercholesterolemic human plasma induces vascular endothelial cell apoptosis by inhibiting fibroblast growth factor 2 transcription. Circulation. 2003; 107: 2102–2108.LinkGoogle Scholar19 Lu J, Jiang W, Yang JH, Chang PY, Walterscheid JP, Chen HH, Marcelli M, Tang D, Lee YT, Liao WS, Yang CY, Chen CH. Electronegative LDL impairs vascular endothelial cell integrity in diabetes by disrupting fibroblast growth factor 2 (FGF2) autoregulation. Diabetes. 2008; 57: 158–166.CrossrefMedlineGoogle Scholar20 Tang D, Lu J, Walterscheid JP, Chen HH, Engler DA, Sawamura T, Chang PY, Safi HJ, Yang CY, Chen CH. Electronegative LDL circulating in smokers impairs endothelial progenitor cell differentiation by inhibiting Akt phosphorylation via LOX-1. J Lipid Res. 2008; 49: 33–47.CrossrefMedlineGoogle Scholar21 Lu J, Yang JH, Burns AR, Chen HH, Tang D, Walterscheid JP, Suzuki S, Yang CY, Sawamura T, Chen CH. Mediation of electronegative low-density lipoprotein signaling by LOX-1: a possible mechanism of endothelial apoptosis. Circ Res. 2009; 104: 619–627.LinkGoogle Scholar22 Voo S, Dunaeva M, Eggermann J, Stadler N, Waltenberger J. Diabetes mellitus impairs CD133+ progenitor cell function after myocardial infarction. J Intern Med. 2009; 265: 238–249.CrossrefMedlineGoogle Scholar23 Schinner S. Wnt-signalling and the metabolic syndrome. Horm Metab Res. 2009; 41: 159–163.CrossrefMedlineGoogle Scholar24 Lee SH, Demeterco C, Geron I, Abrahamsson A, Levine F, Itkin-Ansari P. Islet specific Wnt activation in human type II diabetes. Exp Diabetes Res. 2008; 2008: 728763.MedlineGoogle Scholar25 Kennell JA, Gerin I, MacDougald OA, Cadigan KM. The microRNA miR-8 is a conserved negative regulator of Wnt signaling. Proc Natl Acad Sci U S A. 2008; 105: 15417–15422.CrossrefMedlineGoogle Scholar26 Bonci D, Coppola V, Musumeci M, Addario A, Giuffrida R, Memeo L, D'Urso L, Pagliuca A, Biffoni M, Labbaye C, Bartucci M, Muto G, Peschle C, De Maria R. The miR-15a-miR-16-1 cluster controls prostate cancer by targeting multiple oncogenic activities. Nat Med. 2008; 14: 1271–1277.CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Duan Y, Zhou M, Xiao J, Wu C, Zhou L, Zhou F, Du C and Song Y (2016)(2016) Prediction of key genes and miRNAs responsible for loss of muscle force in patients during an acute exacerbation of chronic obstructive pulmonary disease, International Journal of Molecular Medicine, 10.3892/ijmm.2016.2761, 38:5, (1450-1462), Online publication date: 1-Nov-2016. Chen W, Chen F, Lee A, Ting K, Chang C, Hsu J, Lee W, Sheu J, Chen C and Shen M (2015) Sesamol Reduces the Atherogenicity of Electronegative L5 LDL in Vivo and in Vitro , Journal of Natural Products, 10.1021/np500700z, 78:2, (225-233), Online publication date: 27-Feb-2015. Liu X, Zhang B, McBride J, Zhou K, Lee K, Zhou Y, Liu Z and Ma J (2013) Antiangiogenic and Antineuroinflammatory Effects of Kallistatin Through Interactions With the Canonical Wnt Pathway, Diabetes, 10.2337/db12-1710, 62:12, (4228-4238), Online publication date: 1-Dec-2013. Dai Y, He H, Wise G and Yao S (2011) Hypoxia promotes growth of stem cells in dental follicle cell populations, Journal of Biomedical Science and Engineering, 10.4236/jbise.2011.46057, 04:06, (454-461), . Ascione R and Madeddu P (2009) Risk and Benefit of CD133+ Progenitors, Circulation Research, 105:2, (e2-e2), Online publication date: 17-Jul-2009. May 8, 2009Vol 104, Issue 9 Advertisement Article InformationMetrics https://doi.org/10.1161/CIRCRESAHA.109.198051PMID: 19423862 Originally publishedMay 8, 2009 KeywordsL5WntCD133microRNAdiabetesPDF download Advertisement" @default.
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