Therapeutic Potential of Ex Vivo Expanded Endothelial Progenitor Cells for Myocardial Ischemia

Kawamoto, Atsuhiko; Gwon, Heon-Cheol; Iwaguro, Hideki; Yamaguchi, Junichi; Uchida, Satoshi; Masuda, Haruchika; Silver, Marcy; Ma, Hong; Kearney, Marianne; Isner, Jeffrey M.; Asahara, Takayuki

doi:10.1161/01.cir.103.5.634

Cited by 1,117 publications

(779 citation statements)

References 22 publications

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“…In terms of the functionality of differentiated CD133+ cells, the results seem to be in accordance with a pre-clinical study of Kawamoto et al [22]. In this study, the EPC differentiated in vitro infused in the ischemic area of rats with acute myocardial infarction were found (through posteuthanasia histological study) in the area of neovascularization.…”

Section: Discussionsupporting

confidence: 91%

Formação in vitro de túbulos capilares a partir de células de sangue de cordão umbilical humano com perspectivas para aplicação terapêutica

Senegaglia¹,

Brofman²,

Aita³

et al. 2008

Rev Bras Cir Cardiovasc

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ResumoObjetivo: As células progenitoras endoteliais (CPE), caracterizadas pelo marcador CD133+, contribuem para a neovascularização, e o aumento no número dessas células pode ser uma ferramenta terapêutica promissora. O sangue de cordão umbilical humano contém um número significante de CPE, sugerindo a possibilidade do uso destas células para a revascularização de tecidos isquêmicos. O objetivo desse trabalho foi analisar a funcionalidade das células CD133+ diferenciadas in vitro.Métodos: As células diferenciadas foram caracterizadas 468SENEGAGLIA, AC ET AL -In vitro formation of capillary tubules from human umbilical cord blood cells with perspectives for therapeutic application Bras Cir Cardiovasc 2008; 23(4): 467-473 Rev

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Section: Discussionsupporting

confidence: 91%

Formação in vitro de túbulos capilares a partir de células de sangue de cordão umbilical humano com perspectivas para aplicação terapêutica

Senegaglia¹,

Brofman²,

Aita³

et al. 2008

Rev Bras Cir Cardiovasc

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“…2) Recent reports that arteriogenesis is augmented by bone marrow mononuclear cells [3][4][5] and endothelial progenitor cells suggest involvement in arteriogenesis of not only proliferation of resident cells, but also migration and proliferation of circulating stem cells/precursor cells. [6][7][8] Although previous studies have demonstrated capillary formation (vasculogenesis/angiogenesis) by transplanted cells, [7][8][9][10] they could not demonstrate incorporation of transplanted cells into pre-existing arterioles and arteries, inducing arteriogenesis. In contrast to arteriogenesis, few studies have been conducted examining venogenesis, and little is known about its mechanisms.…”

mentioning

confidence: 94%

Migration of Mononuclear Cells Expressing β-Actin Through the Adventitia into Media and Intima in Coronary Arteriogenesis and Venogenesis in Ischemic Myocardium

Uchida

Maezawa

et al. 2012

Int. Heart J.

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SummaryIt was previously thought that arteriogenesis and venogenesis are induced not only by proliferation of vessel-resident smooth muscle cells (SMCs) and endothelial cells (ECs) but also by migration of their precursors. However, it is not well understood through what route(s) the precursors migrate into the existing vessels.We examined through what route or routes circulating mononuclear cells expressing β-actin (β-MNCs), which we identified in canine coronary vessels, migrate into coronary vessel walls and cause arteriogenesis and venogenesis at 1, 2, 4 and 8 weeks after induction of myocardial infarction.The following changes were observed: (1) The β-MNCs migrated via coronary microvessels to the interstitial space at one week; (2) β-MNCs traversed the adventitia into the media and settled in parallel with pre-existing smooth muscle cells (SMCs) in arterioles and arteries and lost β-actin and acquired α-smooth muscle actin (α-SMA) to become mature SMCs at 2-4 weeks; (3) at the same time, other β-MNCs migrated across the adventitia and media into the intima and settled in parallel with pre-existing endothelial cells (ECs) and lost β-actin, while acquiring CD 31 , to become mature ECs, resulting in arteriogenesis; (4) Similarly, β-MNCs migrated into venular and venous walls and became SMCs or ECs, resulting in venogenesis.β-MNCs in the interstitial space expressed CD 34 but not other major vascular cell markers. β-MNCs, possibly a vascular progenitor, migrate not from the lumen but across the adventitia into the media or intima of coronary vessels and transit to SMCs or ECs, and participate in arteriogenesis and venogenesis in ischemic myocardium. (Int Heart J 2012; 53: 54-63)

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“…Endothelial progenitor cells (EPCs) are bone-marrow derived cells that were first described in 1997 [7]. It has been hypothesised that EPCs play a role in re-endothelialisation of blood vessels damaged by ischaemia [7][8][9][10]. EPCs potentially contribute to endothelial repair by homing into sites of endothelial injury at sites of ischaemia and damage, and thus maintain the integrity of the endothelial milieu.…”

Section: Introductionmentioning

confidence: 99%

Circulating endothelial progenitor cells, endothelial function, carotid intima–media thickness and circulating markers of endothelial dysfunction in people with type 1 diabetes without macrovascular disease or microalbuminuria

et al. 2009

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Aims/hypothesis Type 1 diabetes is associated with premature arterial disease. Bone-marrow derived, circulating endothelial progenitor cells (EPCs) are believed to contribute to endothelial repair. The hypothesis tested was that circulating EPCs are reduced in young people with type 1 diabetes without vascular injury and that this is associated with impaired endothelial function and increased carotid intima-media thickness (CIMT). Methods We compared 74 people with type 1 diabetes with 80 healthy controls. CD34, CD133, vascular endothelial (VE) growth factor receptor-2 (VEGFR-2) and VE-cadherin antibodies were used to quantify EPCs and progenitor cell subtypes using flow-cytometry. Ultrasound assessment of endothelial function by brachial artery flow-mediated dilatation (FMD) and CIMT was made. Circulating endothelial markers, inflammatory markers and plasma plasminogen activator inhibitor-1 (PAI-1) levels were measured. Results CD34+VE-cadherin+, CD133+VE-cadherin+ and CD133+VEGFR-2+ EPC counts were significantly lower in people with diabetes (46-69%; p=0.004-0.043). In people with type 1 diabetes, FMD was reduced by 45% (p<0.001) and CIMT increased by 25% (p<0.001), these being correlated (r=−0.25, p=0.033). There was a significant relationship between FMD and CD34+VE-cadherin+ (r = 0.39, p = 0.001), CD133+VEGFR-2+ (r =0.25, p = 0.037) and CD34+ (r=0.34, p=0.003) counts. Circulating high-sensitivity C-reactive protein, PAI-1, interleukin-6 and E-selectin were significantly higher in the diabetes group (p < 0.001 to p = 0.049), the last two of these correlating with FMD (r=−0.27, p=0.028 and r=−0.24, p=0.048, respectively). Conclusions/interpretation These findings suggest that abnormalities of endothelial function in addition to proinflammatory and pro-thrombotic states are already common in people with type 1 diabetes before development of clinically evident arterial damage. Low EPC counts confirm risk of macrovascular complications and may account for impaired endothelial function and predict future cardiovascular events.

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Therapeutic Potential of Ex Vivo Expanded Endothelial Progenitor Cells for Myocardial Ischemia

Abstract: Ex vivo expanded EPCs incorporate into foci of myocardial neovascularization and have a favorable impact on the preservation of left ventricular function.

Cited by 1,117 publications

References 22 publications

Formação in vitro de túbulos capilares a partir de células de sangue de cordão umbilical humano com perspectivas para aplicação terapêutica

Formação in vitro de túbulos capilares a partir de células de sangue de cordão umbilical humano com perspectivas para aplicação terapêutica

Migration of Mononuclear Cells Expressing β-Actin Through the Adventitia into Media and Intima in Coronary Arteriogenesis and Venogenesis in Ischemic Myocardium

Circulating endothelial progenitor cells, endothelial function, carotid intima–media thickness and circulating markers of endothelial dysfunction in people with type 1 diabetes without macrovascular disease or microalbuminuria

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