Erythropoietin levels in endocrinopathies

J Endocrinol Invest. 2011 Apr 20. [Epub ahead of print]
Erythropoietin levels in endocrinopathies.
Klein E, Brossaud J, Gatta B, Corcuff JB.
Source
Department of Nuclear Medicine, University Hospital of Bordeaux, France.

Background Erythropoietin (EPO) is an oxygen-regulated hormone promoting the differentiation of erythroid progenitor cells. Apart from hypoxia, few data is available about release by secretagogues including hormones. Aim To investigate EPO serum concentration in subjects with endocrine diseases Material and methods A retrospective study evaluating serum EPO concentrations in serum leftovers from subjects with various endocrine disorders Results EPO is not noticeably influenced by thyroid hormone or cortisol concentrations and the relationship with haemoglobin concentration is preserved. In acromegalic patients, the latter is lost but EPO is neither statistically influenced by GH/IGF I. This may reflect a dual action of GH and/or IGF I on erythroid progenitors proliferation as well as on EPO synthesis. Conclusion EPO is not noticeably modified by endocrine disorders although GH and or IGF I may alter EPO relationship with blood haemoglobin concentration.

Pathobiology. 2011;78(1):41-53. Epub 2011 Apr 5.
Erythropoietin: a hormone with multiple functions.
Lombardero M, Kovacs K, Scheithauer BW.
Source
Department of Anatomy and Animal Production, Faculty of Veterinary Sciences, University of Santiago de Compostela, Lugo, Spain.

Erythropoietin (EPO), the main hemopoietic hormone synthesized by the kidney as well as by the liver in fetal life, is implicated in mammalian erythropoiesis. Production and secretion of EPO and the expression of its receptor (EPO-R) are regulated by tissue oxygenation. EPO and EPO-R, expressed in several tissues, exert pleiotropic activities and have different effects on nonhemopoietic cells. EPO is a cytokine with antiapoptotic activity and plays a potential neuroprotective and cardioprotective role against ischemia. EPO is also involved in angiogenesis, neurogenesis, and the immune response. EPO can prevent metabolic alterations, neuronal and vascular degeneration, and inflammatory cell activation. Consequently, EPO may be of therapeutic use for a variety of disorders. Many tumors express EPO and/or EPO-R, but the action of EPO on tumor cells remains controversial. It has been suggested that EPO promotes the proliferation and survival of cancer cells expressing EPO-R. On the other hand, other reports have concluded that EPO-R plays no role in tumor progression. This review provides a detailed insight into the nonhemopoietic role of EPO and its mechanism(s) of action which may lead to a better understanding of its potential therapeutic value in diverse clinical settings

Mol Med Report. 2011 Jan;4(1):31-6. doi: 10.3892/mmr.2010.387. Epub 2010 Oct 21.
Erythropoietin combined with granulocyte colony‑stimulating factor enhances MMP-2 expression in mesenchymal stem cells and promotes cell migration.
Yu Q, Chen L, You Y, Zou C, Zhang Y, Liu Q, Cheng F.
Source
Department of Hematology, Dongfeng Hospital, Yunyang Medical College, Shiyan 442008, P.R. China.

Mesenchymal stem cells (MSCs) are promising clinical tools, but the molecular mechanisms that regulate the mobilization and homing of MSCs and cause invasion through extracellular matrix (ECM) barriers are unknown. Matrix metalloproteinase (MMP) degrades the ECM and promotes cell migration. In this study, we investigated MMP expression and cell migration after treatment with erythropoietin (EPO) and granulocyte colony-stimulating factor (G-CSF). Specifically, we studied whether EPO combined with G-CSF enhanced MMP expression and increased the in vitro motility of MSCs. Real-time PCR was used to detect the mRNA of MMPs and tissue inhibitors of metalloproteinase. Cell migration was evaluated by transwell and wound healing assays. Western blotting was used to detect changes in ERK1/2 protein levels. The results showed that EPO combined with G-CSF enhanced MMP-2 expression in MSCs, promoted MSC motility and activated the ERK1/2 signaling pathway. Thus, a combination treatment of EPO with G-CSF promoted cell migration by stimulating MMP-2 expression in MSCs and this appeared to be related to the ERK1/2 signaling pathway.

Unlike MMP-9, MMP-2 is a pro-hair growth promoting enzyme.