Human periprostatic white adipose tissue is rich in stromal progenitor cells and a potential source of prostate tumor stroma

2012 ◽  
Vol 237 (10) ◽  
pp. 1155-1162 ◽  
Author(s):  
Ricardo Ribeiro ◽  
Cátia Monteiro ◽  
Ricardo Silvestre ◽  
Ângela Castela ◽  
Helena Coutinho ◽  
...  
Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 946-946
Author(s):  
Constance Tom Noguchi ◽  
Heather Marie Rogers ◽  
Li Wang ◽  
Ruifeng Teng

Abstract Erythropoietin is required for erythroid progenitor cell survival, proliferation and differentiation. Increasing evidence suggests that erythropoietin treatment in mice can stimulate erythropoiesis and also affect metabolic processes in a dose dependent manner. For example, medium to high dose erythropoietin treatment (600 U/kg or 3000 U/kg) in leptin deficient obese (ob/ob) mice three times a week for three weeks or more results in the expected increase in hematocrit as well as decrease in accumulated body fat and improved glucose tolerance. Phlebotomy to maintain normal hematocrit demonstrated that erythropoietin regulation of body weight was not dependent on increased red cell mass. In non-obese wild type C57BL/6 mice, erythropoietin treatment also demonstrated the expected increase in hematocrit as well as a 15% reduction in body weight and decreased fasting blood glucose. Erythropoietin receptor is expressed at the highest level in erythroid progenitor cells. The link between increased metabolism and erythropoietin stimulated erythroid differentiation was suggested by the increased oxygen consumption rate observed in vitro in primary cultures of erythropoietin stimulated erythroid progenitor cells. Erythropoietin also stimulated glucose uptake in differentiating erythroid progenitor cells in a dose dependent manner. Glucose uptake decreased with the down regulation of erythropoietin receptor during terminal differentiation. Relatively high erythropoietin receptor expression and erythropoietin activity that may also contribute to erythropoietin metabolic activity has been observed in non-hematopoietic mouse tissue including the hypothalamus and white adipose tissue (Teng R, Gavrilova O et al., Nat Commun 2011). The hypothalamus contributes importantly to appetite regulation and mice treated with erythropoietin exhibited a decrease in food intake compared with saline control. We found that pair-feeding decreased body weight and fat mass, and improved glucose tolerance, but no more than half that observed with erythropoietin treatment, providing evidence that erythropoietin regulation of food intake accounts for only part of the metabolic response observed with erythropoietin treatment. Adipocytes isolated from white adipose tissue in erythropoietin treated mice showed an increase in oxygen consumption compared with vehicle treated or pair-fed mice. To assess the role of direct erythropoietin response of white adipose tissue in regulation of fat mass accumulation, we engineered mice with targeted deletion of erythropoietin receptor in adipose tissue. Erythropoietin treatment gave rise to the expected increase in hematocrit but resulted in a reduced decrease in body weight compared with saline treatment. These data show that erythropoietin treatment can stimulate cell oxygen consumption and can contribute to regulation of metabolism and body weight in mice. Erythropoietin receptor expression on erythroid progenitor cells provides for erythropoietin response to promote erythropoiesis and increase cell metabolic activity including glucose uptake and oxygen consumption. In non-hematopoietic tissue, erythropoietin receptor expression further contributes to erythropoietin regulated metabolic activity such as control of food intake attributed in part to hypothalamus response and modulation of fat mass affected by direct erythropoietin response in white adipose tissue. Therefore, in addition to its critical role in promoting erythropoiesis, erythropoietin can contribute to metabolic homeostasis via its activity in erythroid tissue and beyond. Disclosures: No relevant conflicts of interest to declare.


1996 ◽  
Vol 222 (3) ◽  
pp. 706-712 ◽  
Author(s):  
C. Ribiere ◽  
A.M. Jaubert ◽  
N. Gaudiot ◽  
D. Sabourault ◽  
M.L. Marcus ◽  
...  

2014 ◽  
Vol 298 (5) ◽  
pp. 917-930 ◽  
Author(s):  
Lucio Díaz-Flores ◽  
Ricardo Gutiérrez ◽  
Koldo Lizartza ◽  
Miriam González Goméz ◽  
M. Del Pino García ◽  
...  

2012 ◽  
Vol 72 (20) ◽  
pp. 5198-5208 ◽  
Author(s):  
Yan Zhang ◽  
Alexes C. Daquinag ◽  
Felipe Amaya-Manzanares ◽  
Olga Sirin ◽  
Chieh Tseng ◽  
...  

Obesity ◽  
2012 ◽  
Vol 20 (5) ◽  
pp. 923-931 ◽  
Author(s):  
Wojciech Błogowski ◽  
Mariusz Z. Ratajczak ◽  
Ewelina Żyżniewska-Banaszak ◽  
Barbara Dołęgowska ◽  
Teresa Starzyńska

Author(s):  
Rohollah Babaei ◽  
Irem Bayindir-Buchhalter ◽  
Irina Meln ◽  
Alexandros Vegiopoulos

2016 ◽  
Author(s):  
Rokhsareh Rohban ◽  
Nathalie Etchart ◽  
Thomas R. Pieber

AbstractIt has been believed that de novo vessel formation (neo-vasculogenesis) can be induced by co-transplantation of pericytes or mesenchymal stem/progenitor cells (MSPC) with endothelial cells or endothelial colony-forming cells (ECFC). The requirement for co-transplantation of two adult progenitor cells is one factor that can potentially complicate the process of therapeutic vasculogenesis which hampers the development of strategies for therapeutic intervention referred to as ‘regenerative medicine’. Here we employed a novel strategy for therapeutic vessel development by transplanting endothelial colony forming progenitor cells solely to immune compromised mice and detect vessel formation capacity of single ECFC transplants compared to ECFC/MSPC co-transplants. We applied umbilical cord derived and bone marrow derived-MSPC and umbilical cord derived ECFC with different total cell number for subcutaneous transplantation in matrix composites either alone or mixed at a ratio of 1:5 subcutaneously into immune deficient NOD.Cg-Prkdcscid Il2rgtm1Wjl/SzJ; NSG mice. Implants were harvested one day, one, two, eight and 24 weeks after transplantation for detecting the state of vessel formation and stability of the transplants by histological assessments. Additionally, endothelial progenitor cells derived from various human tissues such as umbilical cord blood, peripheral blood and white adipose tissue were used to assess their potential for vessel formation in vivo.Results confirmed that single transplantation of ECFCs with a higher cell number and later in the time course after transplantation is as efficient as co-transplantation of ECFC with MSPC at forming stable-perfused human vessels. Amongst ECFCs isolated from different human sources, white adipose tissue derived ECFC are most potent in forming neo-vessels (micro-vessels) in vivo, thus WAT-ECFC could be an optimal cell for vasculogenesis regenerative application.Co-transplantation of ECFC and MSPC with the defined 5:1 ratio or sole ECFC with a higher cell dosage was essential for vessel generation in vivo.


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