Effect of recombinant human erythropoietin on endothelial cell apoptosis

Carlini, Raúl G.; Alonzo, Evelyn; Domínguez, José Ramón Fernández; Blanca, Isaac; Weisinger, José R.; Rothstein, Marcos; Bellorín-Font, Ezequiel

doi:10.1046/j.1523-1755.1999.00266.x

Cited by 103 publications

(73 citation statements)

References 21 publications

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“…CD34+/Flk-1 (also known KDR or VEGFR2) positive cells are hematopoietic progenitor cells that may differentiate into endothelial cells and contribute to neovascularization and vascular repair (197,198). Epo promotes proliferation (40,196), inhibits apoptosis (199), and facilitates differentiation of EPCs (200)(201)(202)(203). Furthermore, Epo induces mobilization of EPCs into the circulation (204,205), and their homing (155,206,207).…”

Section: Epo In Treatment Of Cardiovascular Diseasesmentioning

confidence: 99%

Epo and Non-hematopoietic Cells: What Do We Know?

Ogunshola

Bogdanova

2013

Methods in Molecular Biology

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Section: Epo In Treatment Of Cardiovascular Diseasesmentioning

confidence: 99%

Epo and Non-hematopoietic Cells: What Do We Know?

Ogunshola

Bogdanova

2013

Methods in Molecular Biology

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“…51 Erythropoietin has been shown to inhibit apoptosis in cultured bovine aortic endothelial cells in response to endotoxin. 52 Initial experience with aurintricarboxylic acid, a potent inhibitor of apoptosis, indicates that it inhibits TTP-plasma induced endothelial apoptosis in vitro, but its toxicity appears to preclude its clinical use. 53 TNF␣ appears to be an important cytokine mediator of GVHD and may also be important in the initiation of TA-TMA.…”

Section: Future Directions In Diagnosis and Management Of Ta-tmamentioning

confidence: 99%

Transplantation-associated thrombotic microangiopathy: twenty-two years later

Daly

Xenocostas

Lipton

2002

Bone Marrow Transplant

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Summary:A syndrome of microangiopathic hemolytic anemia, renal dysfunction and neurological abnormalities was first noted in bone marrow transplant recipients 22 years ago. Now known as transplantation-associated thrombotic microangiopathy (TA-TMA) to distinguish it from other thrombotic microangiopathies, this disorder responds poorly to conventional treatments for thrombotic thrombocytopenic purpura. In this review, we discuss the incidence and risk factors for TA-TMA and describe a pathophysiologic model of the disorder based on results obtained from laboratory models of the thrombotic microangiopathies. We conclude by suggesting possible approaches to the early diagnosis and treatment of TA-TMA based on this model that may warrant testing in future clinical trials.

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“…Several studies have suggested that Epo might stimulate angiogenesis by acting to promote proliferation and/or migration of endothelial cells (Anagnostou et al, 1990;Ribatti et al, 1999), inhibiting apoptosis of endothelial cells (Carlini et al, 1999), or by increasing MMP-2 secretion (Ribatti et al, 1999). rEpo has also been shown to increase the number of circulating endothelial cells and endothelial cell progenitors in preclinical models (Monestiroli et al, 2001) and human breast cancer and lymphoma models ).…”

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confidence: 99%

Human recombinant erythropoietin (rEpo) has no effect on tumour growth or angiogenesis

et al. 2005

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Tumour hypoxia has been shown to increase mutation rate, angiogenesis, and metastatic potential, and decrease response to conventional therapeutics. Improved tumour oxygenation should translate into increased treatment response. Exogenous recombinant erythropoietin (rEpo) has been recently shown to increase tumour oxygenation in a mammary carcinoma model. The mechanism of this action is not yet understood completely. The presence of Epo and its receptor (EpoR) have been demonstrated on several normal and neoplastic tissues, including blood vessels and various solid tumours. In addition, rEpo has been shown in two recent prospective, randomized clinical trials to negatively impact treatment outcome. In this study, we attempt to characterize the direct effects of rEpo on tumour growth and angiogenesis in two separate rodent carcinomas. The effect of rEpo on R3230 rat mammary adenocarcinomas, CT-26 mouse colon carcinomas, HCT-116 human colon carcinomas, and FaDu human head and neck tumours, all of which express EpoR, was examined. There were no differences in tumour growth or proliferation (measured by Ki-67) between placebo-treated and rEpo-treated tumours. In the mammary window chamber, vascular length density (VLD) measurements in serial images of both placebo-treated and Epo-treated rats revealed no difference in angiogenesis between the Epo-treated tumours and placebo-treated tumours at any time point. These experiments are important because they suggest that the recent clinical detriment seen with the use of Epo is not due to its tumour growth effects or angiogenesis. These studies also suggest that further preclinical studies need to examine rEpo's direct tumour effects in efforts to improve the therapeutic benefits of Epo in solid tumour patients.

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Effect of recombinant human erythropoietin on endothelial cell apoptosis

Abstract: These results suggest that rHuEPO prevents LPS-induced apoptosis in endothelial cells. This protective effect could be an important factor in the action of rHuEPO on vascular endothelium.

Cited by 103 publications

References 21 publications

Epo and Non-hematopoietic Cells: What Do We Know?

Epo and Non-hematopoietic Cells: What Do We Know?

Transplantation-associated thrombotic microangiopathy: twenty-two years later

Human recombinant erythropoietin (rEpo) has no effect on tumour growth or angiogenesis

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