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利用重编程造血祖细胞进行钻石黑范贫血的药物发现。

Drug discovery for Diamond-Blackfan anemia using reprogrammed hematopoietic progenitors.

作者信息

Doulatov Sergei, Vo Linda T, Macari Elizabeth R, Wahlster Lara, Kinney Melissa A, Taylor Alison M, Barragan Jessica, Gupta Manav, McGrath Katherine, Lee Hsiang-Ying, Humphries Jessica M, DeVine Alex, Narla Anupama, Alter Blanche P, Beggs Alan H, Agarwal Suneet, Ebert Benjamin L, Gazda Hanna T, Lodish Harvey F, Sieff Colin A, Schlaeger Thorsten M, Zon Leonard I, Daley George Q

机构信息

Division of Hematology/Oncology, Boston Children's Hospital and Dana Farber Cancer Institute, Boston, MA 02115, USA.

Stem Cell Program, Boston Children's Hospital, Boston, MA 02115, USA.

出版信息

Sci Transl Med. 2017 Feb 8;9(376). doi: 10.1126/scitranslmed.aah5645.

Abstract

Diamond-Blackfan anemia (DBA) is a congenital disorder characterized by the failure of erythroid progenitor differentiation, severely curtailing red blood cell production. Because many DBA patients fail to respond to corticosteroid therapy, there is considerable need for therapeutics for this disorder. Identifying therapeutics for DBA requires circumventing the paucity of primary patient blood stem and progenitor cells. To this end, we adopted a reprogramming strategy to generate expandable hematopoietic progenitor cells from induced pluripotent stem cells (iPSCs) from DBA patients. Reprogrammed DBA progenitors recapitulate defects in erythroid differentiation, which were rescued by gene complementation. Unbiased chemical screens identified SMER28, a small-molecule inducer of autophagy, which enhanced erythropoiesis in a range of in vitro and in vivo models of DBA. SMER28 acted through autophagy factor ATG5 to stimulate erythropoiesis and up-regulate expression of globin genes. These findings present an unbiased drug screen for hematological disease using iPSCs and identify autophagy as a therapeutic pathway in DBA.

摘要

先天性纯红细胞再生障碍性贫血(DBA)是一种先天性疾病,其特征是红系祖细胞分化失败,严重减少红细胞生成。由于许多DBA患者对皮质类固醇治疗无反应,因此对这种疾病的治疗方法有很大需求。确定DBA的治疗方法需要克服原发性患者血液干细胞和祖细胞的稀缺性。为此,我们采用了一种重编程策略,从DBA患者的诱导多能干细胞(iPSC)中生成可扩增的造血祖细胞。重编程的DBA祖细胞重现了红系分化缺陷,通过基因互补得以挽救。无偏倚化学筛选鉴定出SMER28,一种自噬小分子诱导剂,它在一系列DBA的体外和体内模型中增强了红细胞生成。SMER28通过自噬因子ATG5发挥作用,刺激红细胞生成并上调珠蛋白基因的表达。这些发现展示了使用iPSC对血液疾病进行无偏倚药物筛选,并确定自噬是DBA的一种治疗途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/984b/5501179/986914435037/nihms867182f1.jpg

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