Direct effect of erythropoietin on rat vascular smooth-muscle cell via a putative erythropoietin receptor

Ammarguellat, Fatima; Gogusev, Jean; Drüeke, Tilman B.

doi:10.1093/oxfordjournals.ndt.a027361

Cited by 86 publications

(58 citation statements)

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“…Epo is known to have effects not only in erythropoiesis and thrombopoiesis 21,22 but also on many other cells and tissues, including endothelial cells, 26 smooth muscle cells, 27,28 cardiomyocytes, 29 and kidney cells, 30 as well as neuroprotective and suppressive actions in ischemia-induced neuronal cell death as neurogenic and neuroprotective agents via antiapoptotic, neurotrophic, antioxidant, and angiogenic effects. 10,13,31,32 Our study, however, showed that brain weight was significantly reduced in the Epoetin-treated group as compared with Epo-bp-and ␣Epo-bp-treated groups ( Table 1).…”

Section: Discussionmentioning

confidence: 99%

Prevention of Erythropoietin-Associated Hypertension

Lee

2007

Hypertension

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Abstract-Hypertension is the most significant complication from treatment with erythropoietin (Epo). Can Epo-induced hypertension be eliminated? We examined systemic and local effects of our genetically engineered products, Epo-binding protein (Epo-bp) and anti-Epo-bp antibodies, on randomly assigned Sprague-Dawley rats at midnight, 4 AM, 8 AM, noon, 4 PM, and 8 PM. Blood pressure, hematocrit, and body weight were measured immediately before and after the completion of a 4-week, twice-weekly course of Epo (50 U/kg), Epo-bp, anti-Epo-bp antibodies, or physiological saline injections. Epo treatment increased hematocrit markedly overall as compared with the saline, Epo-bp, and anti-Epo-bp antibody groups (0.616 versus 0.427, 0.439, and 0.441, respectively) and at each of the 6 test times (all PϽ0.0001). Epo-bp and anti-Epo-bp antibody treatment with Epo had almost no effect on the Epo-induced hematocrit increase (0.616 versus 0.580 or 0.591, respectively

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Section: Discussionmentioning

confidence: 99%

Prevention of Erythropoietin-Associated Hypertension

Lee

2007

Hypertension

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“…Functional EpoR expression has been documented in many nonhematopoietic cell types, including vascular endothelial cells (20), smooth muscle cells (21), skeletal myoblasts (22), cardiac myocytes (23), neurons (24), retinal photoreceptors (25), liver stromal cells (26), placenta (27), kidney (28), and macrophages (29). EpoR expression and signaling in hematopoietic tissues is essential for normal mammalian erythropoiesis during development.…”

Section: Expression and Function Of Epo And Its Receptormentioning

confidence: 99%

Erythropoietin Biology in Cancer

Hardee¹,

Arcasoy

Blackwell

et al. 2006

Clinical Cancer Research

195

163

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Erythropoietin (Epo) has long been known to be the principal hematopoietic growth factor that regulates cellular proliferation and differentiation along the erythroid lineage. Recent studies have shown that Epo is a pleiotropic cytokine that is proangiogenic and exerts broad tissue-protective effects in diverse nonhematopoietic organs. Recombinant Epo (rEpo) has been widely used in the clinic to prevent or treat malignancy-associated anemia. A series of clinical trials have documented the efficacy of rEpo in reducing RBC transfusion requirements and improving quality of life in cancer patients, and a recent meta-analysis suggested a positive effect on survival. However, two randomized trials reported negative outcomes with rEpo, as patients in the rEpo arm fared worse than their placebo-treated counterparts with respect to progression-free survival. The expression of Epo receptor (EpoR) in cancer cells has raised the possibility that exogenous rEpo may exert direct effects on tumor cells associated with the potential for stimulation of proliferation, inhibition of apoptosis, or modulation of sensitivity to chemoradiation therapy.The presence of an autocrine-paracrine Epo-EpoR system in tumors and potential effects of Epo on tumor microenvironment and angiogenesis are consistent with a complex biology for Epo-EpoR signaling in cancer that requires further research.This review describes Epo and EpoR biology, focusing on the pleiotropic effects of Epo on nonhematopoietic tissues as well as the expression and function of EpoR in cancer cells.

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“…Erythropoietin (EPO), a cytokine that was originally identified as a hematopoietic factor, has been widely used for the treatment of anemia in patients with chronic kidney diseases for nearly 20 yr. 8 More recently, EPO was found to interact with its receptor, expressed in a great variety of nonhematopoietic cell types (e.g., neurons, 9 endothelial cells, 10 vascular smooth muscle cells, 11 cardiomyocytes, 12 mesangial cells, renal proximal tubular cells 13 ) to induce a range of cytoprotective cellular responses (mitogenesis, 13 angiogenesis, 14 promotion of vas-cular repair, 15 and inhibition of apoptosis 16,17 ), which are independent of EPO's effects on erythropoiesis. 18 Indeed, EPO was reported to attenuate renal injury in acute renal failure models in experimental animals with ischemia-reperfusion, 19,20 cisplatin, 21 and radiocontrast medium injuries.…”

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confidence: 99%

Asialoerythropoietin Prevents Contrast-Induced Nephropathy

Yokomaku¹,

Sugimoto²,

Kume³

et al. 2008

Journal of the American Society of Nephrology

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Strategies to prevent contrast-induced nephropathy (CIN) are suboptimal. Erythropoietin was recently found to be cytoprotective in a variety of nonhematopoietic cells, so it was hypothesized that the nonhematopoietic erythropoietin derivative asialoerythropoietin would prevent CIN. Nephropathy was induced in rats by injection of the radiocontrast medium Ioversol in addition to inhibition of prostaglandin and nitric oxide synthesis. Administration of a single dose of asialoerythropoietin before the induction of nephropathy significantly attenuated the resulting renal dysfunction and histologic renal tubular injury. Contrast-induced apoptosis of renal tubular cells was inhibited by asialoerythropoietin both in vivo and in vitro, and this effect was blocked by a Janus kinase 2 (JAK2) inhibitor in vitro. Furthermore, phospho-JAK2/signal transducer and activator of transcription 5 (STAT5) and heat-shock protein 70 increased after injection of asialoerythropoietin, suggesting that the effects of asialoerythropoietin may be mediated by the activation of the JAK2/STAT5 pathway. Overall, these findings suggest that asialoerythropoietin may have potential as a new therapeutic approach to prevent CIN given its ability to preserve renal function and directly protect renal tissue.

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Direct effect of erythropoietin on rat vascular smooth-muscle cell via a putative erythropoietin receptor

Abstract: The present report provides preliminary evidence in favour of a direct action of the hormone on vascular smooth muscle via a specific EpoR.

Cited by 86 publications

References 0 publications

Prevention of Erythropoietin-Associated Hypertension

Prevention of Erythropoietin-Associated Hypertension

Erythropoietin Biology in Cancer

Asialoerythropoietin Prevents Contrast-Induced Nephropathy

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