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5/2012 vol. 50
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PRACA PRZEGLĄDOWA
Rola endotelialnych komórek progenitorowych i potencjału redoks w neowaskularyzacji błony maziowej stawu
Przemysław Rzodkiewicz
,
 
Michał Gajewski
,
 
Sławomir Maśliński
,
 
Elżbieta Wojtecka-Łukasik
 
 
 
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Ukryj
 
Data publikacji online: 06-11-2012
 
 
Reumatologia 2012;50(5):432-437
DOI: https://doi.org/10.5114/reum.2012.31406
 
 
Artykuł (PDF)
Referencje (41)
 
SŁOWA KLUCZOWE
neowaskularyzacja błony maziowej
NADPH oksydaza
redoks
endotelialne progenitorowe komórki macierzyste
 
STRESZCZENIE
Zwiększona neowaskularyzacja błony maziowej jest jednym z istotnych elementów patomechanizmu rozwoju reumatoidalnego zapalenia stawów (RZS). Jednym z czynników mających znaczenie w przebiegu tego procesu jest produkcja wolnych rodników tlenowych, które wpływają zarówno na proces neowaskularyzacji, jak i na metabolizm endotelialnych komórek progenitorowych. Zaburzenia związane z produkcją wolnych rodników tlenowych w przebiegu zapalenia mogą być więc nie tylko bezpośrednią przyczyną uszkodzeń obserwowanych w przebiegu RZS, lecz także czynnikiem wpływającym na przebieg choroby. W niniejszej publikacji przedstawiono stan aktualnej wiedzy na temat procesu neowaskularyzacji, ze szczególnym omówieniem znaczenia potencjału redoks.
 
REFERENCJE (41)
1.
Kotulska A, Kucharz JE. Angiogeneza w reumatoidalnym zapaleniu stawów. Reumatologia 2011; 49: 1-9.
Google Scholar
 
 
2.
Szekanecz Z, Besenyei T, Paragh G, Koch AE. Angiogenesis in rheumatoid arthritis. Autoimmunity 2009; 42: 563-573.
Google Scholar
 
 
3.
Szekanecz Z, Pakozdi A, Szentpetery A, et al. Chemokines and angiogenesis in rheumatoid arthritis. Front Biosci (Elite Ed) 2009; 1: 44-51.
Google Scholar
 
 
4.
Głowińska-Olszewska B, Łuczyński W, Bossowski A. Komórki progenitorowe śródbłonka jako nowy marker funkcji endotelium w ocenie ryzyka chorób układu sercowo-naczyniowego. Postepy Hig Med Dosw 2011; 65: 8-15.
Google Scholar
 
 
5.
Zampetaki A, Kirton JP, Xu Q. Vascular repair by endothelial progenitor cells. Cardiovasc Res 2008; 78: 413-421.
Google Scholar
 
 
6.
Medina RJ, O’Neill CL, Sweeney M, et al. Molecular analysis of endothelial progenitor cell (EPC) subtypes reveals two distinct cell populations with different identities. BMC Med Genomics 2010; 3: 18.
Google Scholar
 
 
7.
Skóra J, Biegus J, Pupka A i wsp. Molekularne podstawy angiogenezy. Postepy Hig Med Dosw 2006; 60: 410-415.
Google Scholar
 
 
8.
Urbich C, Dimmeler S. Endothelial progenitor cells characterization and role in vascular biology. Circ Res 2004; 95: 343-353.
Google Scholar
 
 
9.
Aicher A, Heeschen C, Mildner-Rihm C, et al. Essential role of endothelial nitric oxide synthase for mobilization of stem and progenitor cells. Nat Med 2003; 9: 1370-1376.
Google Scholar
 
 
10.
Foubert P, Silvestre JS, Souttou B, et al. PSGL-1-mediated activation of EphB4 increases the proangiogenic potential of endothelial progenitor cells. J Clin Invest 2007; 117: 1527-1537.
Google Scholar
 
 
11.
Duan H, Cheng L, Sun X, et al. LFA-1 and VLA-4 involved in human high proliferative potential-endothelial progenitor cells homing to ischemic tissue. Thromb Haemost 2006; 96: 807-815.
Google Scholar
 
 
12.
Wang H, Riha GM, Yan S, et al. Shear stress induces endothelial differentiation from a murine embryonic mesenchymal progenitor cell line. Arterioscler Thromb Vasc Biol 2005; 25: 1817-1823.
Google Scholar
 
 
13.
Rössig L, Urbich C, Brühl T, et al. Histone deacetylase activity is essential for the expression of HoxA9 and for endothelial commitment of progenitor cells. J Exp Med 2005; 201: 1825-1835.
Google Scholar
 
 
14.
Urbich C, Aicher A, Heeschen C, et al. Soluble factors released by endothelial progenitor cells promote migration of endothelial cells and cardiac resident progenitor cells. J Mol Cell Cardiol 2005; 39: 733-742.
Google Scholar
 
 
15.
Rüger B, Giurea A, Wanivenhaus AH, et al. Endothelial precursor cells in the synovial tissue of patients with rheumatoid arthritis and osteoarthritis. Arthritis Rheum 2004; 50: 2157-2166.
Google Scholar
 
 
16.
Hirohata S, Yanagida T, Nampei A, et al. Enhanced generation of endothelial cells from CD34þ cells of the bone marrow in rheumatoid arthritis: possible role in synovial neovascularization. Arthritis Rheum 2004; 50: 3888-3896.
Google Scholar
 
 
17.
Herbrig K, Haensel S, Oelschlaegel U, et al. Endothelial dysfunction in patients with rheumatoid arthritis is associated with a reduced number and impaired function of endothelial progenitor cells. Ann Rheum Dis 2006; 65: 157-163.
Google Scholar
 
 
18.
Grisar J, Aletaha D, Steiner CW, et al. Depletion of endothelial progenitor cells in the peripheral blood of patients with rheumatoid arthritis. Circulation 2005; 111: 204-211.
Google Scholar
 
 
19.
Ablin JN, Boguslavski V, Aloush V, et al. Effect of anti-TNFαlpha treatment on circulating endothelial progenitor cells (EPCs) in rheumatoid arthritis. Life Sci 2006; 79: 2364-2369.
Google Scholar
 
 
20.
Grisar J, Aletaha D, Steiner CW, et al. Endothelial progenitor cells in active rheumatoid arthritis: effects of TNF and of glucocorticoid therapy. Ann Rheum Dis 2007; 66: 1284-1288.
Google Scholar
 
 
21.
Avouac J, Uzan G, Kahan A, et al. Endothelial progenitor cells and rheumatic disorders. Joint Bone Spine 2008; 75: 131-137.
Google Scholar
 
 
22.
Henrotin YE, Bruckner P, Pujol JP. The role of reactive oxygen species in homeostasis and degradation of cartilage. Osteoarthritis Cartilage 2003; 11: 747-755.
Google Scholar
 
 
23.
Gajewski M, Rzodkiewicz P, Maśliński S. Aktualne poglądy na znaczenie neutrofilów w reumatoidalnym zapaleniu stawów. Wciąż neutrofile czy może już mikrofagi? Reumatologia 2011; 49: 344-350.
Google Scholar
 
 
24.
Chi PL, Chen YW, Hsiao LD, et al. Heme oxygenase 1 attenuates interleukin-1-induced cytosolic phospholipase A2 expression via a decrease in NADPH oxidase/reactive oxygen species/activator protein 1 activation in rheumatoid arthritis synovial fibroblasts. Arthritis Rheum 2012; 64: 2114-2125.
Google Scholar
 
 
25.
Ushio-Fukai M, Urao N. Novel role of NADPH oxidase in angiogenesis and stem/progenitor cell function. Antioxid Redox Signal 2009; 11: 2517-2533.
Google Scholar
 
 
26.
Dröge W. Free radicals in the physiological control of cell function. Physiol Rev 2002; 82: 47-95.
Google Scholar
 
 
27.
Tojo T, Ushio-Fukai M, Yamaoka-Tojo M, et al. Role of gp91phox (Nox2)-containing NAD(P)H oxidase in angiogenesis in response to hindlimb ischemia. Circulation 2005; 111: 2347-2355.
Google Scholar
 
 
28.
Ushio-Fukai M, Tang Y, Fukai T, et al. Novel role of gp91(phox)-containing NAD(P)H oxidase in vascular endothelial growth factor-induced signaling and angiogenesis. Circ Res 2002; 91: 1160-1167.
Google Scholar
 
 
29.
Higai K, Shimamura A, Matsumoto K. Amadori-modified glycated albumin predominantly induces E-selectin expression on human umbilical vein endothelial cells through NADPH oxidase activation. Clin Chim Acta 2006; 367: 137-143.
Google Scholar
 
 
30.
Min JK, Kim YM, Kim SW, et al. TNF-related activation induced cytokine enhances leukocyte adhesiveness: induction of ICAM-1 and VCAM-1 via TNF receptor-associated factor and protein kinase C-dependent NF-kappaB activation in endothelial cells. J Immunol 2005; 175: 531-540.
Google Scholar
 
 
31.
Akgür FM, Brown MF, Zibari GB, et al. Role of superoxide in hemorrhagic shock-induced P-selectin expression. Am J Physiol Heart Circ Physiol 2000; 279: H791-797.
Google Scholar
 
 
32.
Ebrahimian TG, Heymes C, You D, et al. NADPH oxidase-derived overproduction of reactive oxygen species impairs postischemic neovascularization in mice with type 1 diabetes. Am J Pathol 2006; 169: 719-728.
Google Scholar
 
 
33.
Urao N, Inomata H, Razvi M, et al. Role of nox2-based NADPH oxidase in bone marrow and progenitor cell function involved in neovascularization induced by hindlimb ischemia. Circ Res 2008; 103: 212-220.
Google Scholar
 
 
34.
Fuhler GM, Drayer AL, Olthof SG, et al. Reduced activation of protein kinase B, Rac, and F-actin polymerization contributes to an impairment of stromal cell derived factor-1 induced migration of CD34+ cells from patients with myelodysplasia. Blood 2008; 111: 359-368.
Google Scholar
 
 
35.
Zhao M, Wimmer A, Trieu K, et al. Arrestin regulates MAPK activation and prevents NADPH oxidase-dependent death of cells expressing CXCR2. J Biol Chem 2004; 279: 49259-49267.
Google Scholar
 
 
36.
Hristov M, Zernecke A, Bidzhekov K, et al. Importance of CXC chemokine receptor 2 in the homing of human peripheral blood endothelial progenitor cells to sites of arterial injury. Circ Res 2007; 100: 590-597.
Google Scholar
 
 
37.
Olsson LM, Lindqvist AK, Källberg H, et al. A case-control study of rheumatoid arthritis identifies an associated single nucleotide polymorphism in the NCF4 gene, supporting a role for the NADPH-oxidase complex in autoimmunity. Arthritis Res Ther 2007; 9: R98.
Google Scholar
 
 
38.
Olofsson P, Holmberg J, Tordsson J, et al. Positional identification of Ncf1 as a gene that regulates arthritis severity in rats. Nat Genet 2003; 33: 25-32.
Google Scholar
 
 
39.
Hultqvist M, Olofsson P, Holmberg J, et al. Enhanced autoimmunity, arthritis, and encephalomyelitis in mice with a reduced oxidative burst due to a mutation in the Ncf1 gene. Proc Natl Acad Sci U S A 2004; 101: 12646-12651.
Google Scholar
 
 
40.
Gelderman KA, Hultqvist M, Holmberg J, et al. T cell surface redox levels determine T cell reactivity and arthritis susceptibility. Proc Natl Acad Sci U S A 2006; 103: 12831-12836.
Google Scholar
 
 
41.
Reth M. Hydrogen peroxide as second messenger in lymphocyte activation. Nat Immunol 2002; 3: 1129-1134.
Google Scholar
 
 
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