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10.1038/nm.4477 http://scihub22266oqcxt.onion/10.1038/nm.4477 C5875416!5875416 !29377004     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29377004 &cmd=llinks): Failed to open stream: HTTP request failed! 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Antagonism of PPAR-? signaling expands human hematopoietic stem and progenitor cells by enhancing glycolysis |pdf=|usr=}}{{29377004 }} gab.com Text Antagonism of PPAR- signaling expands human hematopoietic stem and progenitor cells by enhancing glycolysis JO: Nat Med http://www.kidney.de/pget.php?&tw=1&pmid=29377004 #FOAvip Hematopoietic stem cells (HSCs) quiescently reside in bone marrow niches and have the capacity to self-renew or differentiate to form all of the blood cells throughout the lifespan of an animal. Allogeneic HSC transplantation is a life-saving treatment for malignant and nonmalignant disorders. HSCs isolated from umbilical cord blood (CB) are used for hematopoietic cell transplantation (HCT), but due to the limited numbers of HSCs in single units of umbilical CB, a number of methods have been proposed for ex vivo expansion of human HSCs. We show here that antagonism of peroxisome proliferator-activated receptor (PPAR)-? promotes ex vivo expansion of phenotypically and functionally defined subsets of human CB HSCs and hematopoietic progenitor cells (HSPCs). PPAR-? antagonism in CB HSPCs strongly downregulated expression of several differentiation-associated genes, as well as fructose-bisphosphatase 1 (FBP1; which encodes a negative regulator of glycolysis), and enhanced glycolysis without compromising mitochondrial metabolism. The expansion of CB HSPCs by PPAR-? antagonism was completely suppressed by removal of glucose or inhibition of glycolysis. Moreover, knockdown of FBP1 expression promoted glycolysis and ex vivo expansion of long-term repopulating CB HSPCs, whereas overexpression of FBP1 suppressed the expansion of CB HSPCs that was induced by PPAR-? antagonism. Our study suggests the possibility for a new and simple means for metabolic reprogramming of CB HSPCs to improve the efficacy of HCT. Twit Text FOAVip Antagonism of PPAR- signaling expands human hematopoietic stem and progenitor cells by enhancing glycolysis ????Nat Med http://www.kidney.de/pget.php?&tw=1&pmid=29377004 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29377004 #FOAvip English Wikipedia <ref>{{Cite pmid|29377004 }}</ref> Antagonism of PPAR-? signaling expands human hematopoietic stem and progenitor cells by enhancing glycolysis #MMPMID29377004 Guo B ; Huang X ; Lee MR ; Lee SA ; Broxmeyer HE Nat Med 2018[Mar]; 24 (3 ): 360-367 PMID29377004 show ga Hematopoietic stem cells (HSCs) quiescently reside in bone marrow niches and have the capacity to self-renew or differentiate to form all of the blood cells throughout the lifespan of an animal. Allogeneic HSC transplantation is a life-saving treatment for malignant and nonmalignant disorders. HSCs isolated from umbilical cord blood (CB) are used for hematopoietic cell transplantation (HCT), but due to the limited numbers of HSCs in single units of umbilical CB, a number of methods have been proposed for ex vivo expansion of human HSCs. We show here that antagonism of peroxisome proliferator-activated receptor (PPAR)-? promotes ex vivo expansion of phenotypically and functionally defined subsets of human CB HSCs and hematopoietic progenitor cells (HSPCs). PPAR-? antagonism in CB HSPCs strongly downregulated expression of several differentiation-associated genes, as well as fructose-bisphosphatase 1 (FBP1; which encodes a negative regulator of glycolysis), and enhanced glycolysis without compromising mitochondrial metabolism. The expansion of CB HSPCs by PPAR-? antagonism was completely suppressed by removal of glucose or inhibition of glycolysis. Moreover, knockdown of FBP1 expression promoted glycolysis and ex vivo expansion of long-term repopulating CB HSPCs, whereas overexpression of FBP1 suppressed the expansion of CB HSPCs that was induced by PPAR-? antagonism. Our study suggests the possibility for a new and simple means for metabolic reprogramming of CB HSPCs to improve the efficacy of HCT. |Cell Differentiation/genetics [MESH] |Cell Lineage/genetics [MESH] |Fetal Blood/cytology/metabolism [MESH] |Fructose-Bisphosphatase/genetics [MESH] |Gene Expression Regulation, Developmental [MESH] |Gene Knockdown Techniques [MESH] |Glycolysis/*genetics [MESH] |Hematopoietic Stem Cell Transplantation [MESH] |Hematopoietic Stem Cells/cytology/*metabolism [MESH] |Humans [MESH] |PPAR gamma/antagonists & inhibitors/*genetics [MESH] |Signal Transduction/genetics [MESH]Antagonism of PPAR-? signaling expands human hematopoietic stem and pr(epmc).pdf DeepDyve Pubget Overpricing