Literature DB >> 30984818

Human beta cells generated from pluripotent stem cells or cellular reprogramming for curing diabetes.

Lauren N Randolph1,2, Agamoni Bhattacharyya1,2, Xiaojun Lance Lian1,2,3.   

Abstract

Diabetes is a group of metabolic diseases characterized by aberrantly high blood glucose levels caused by defects in insulin secretion, its action, or both, which affects approximately 30.3 million people (9.4% of the population) in the United States. This review will focus on using human β cells to treat and cure diabetes because β cells are absent, due to an autoimmune destruction, in Type 1 diabetes or dysfunctional in Type 2 diabetes. In order to generate enough functional β cells for diabetes treatment (0.1 to 1 billion cells to treat one patient), a basic science approach by mimicking what happens in normal pancreatic development must be closely aligned with engineering. Two general approaches are discussed here. The first one uses human pluripotent stem cells (hPSCs) to perform directed differentiation of hPSCs to β cells. This is advantageous because hPSCs grow indefinitely, providing a virtually unlimited source of material. Therefore, if we develop an efficient β cell differentiation protocol, we can essentially generate an unlimited amount of β cells for disease modeling and diabetes treatment. The second approach is cellular reprogramming, with which we may begin with any cell type and covert it directly into a β cell. The success of this cellular reprogramming approach, however, depends on the discovery of a robust and efficient transcription factor cocktail that can ignite this process, similar to what has been achieved in generating induced pluripotent stem cells. This discovery should be possible through identifying the important transcription factors and pioneer factors via recent advances in single-cell RNA sequencing. In short, a new renaissance in pancreas developmental biology, stem cell engineering, and cellular reprogramming for curing diabetes appears to be on the horizon.

Entities:  

Year:  2018        PMID: 30984818      PMCID: PMC6457681          DOI: 10.1007/s40883-018-0082-y

Source DB:  PubMed          Journal:  Regen Eng Transl Med        ISSN: 2364-4141


  52 in total

1.  Mosaic Cre-mediated recombination in pancreas using the pdx-1 enhancer/promoter.

Authors:  M Gannon; P L Herrera; C V Wright
Journal:  Genesis       Date:  2000-02       Impact factor: 2.487

2.  Differentiation of embryonic stem cells to insulin-secreting structures similar to pancreatic islets.

Authors:  N Lumelsky; O Blondel; P Laeng; I Velasco; R Ravin; R McKay
Journal:  Science       Date:  2001-04-26       Impact factor: 47.728

3.  Pancreatic and duodenal homeobox gene 1 induces expression of insulin genes in liver and ameliorates streptozotocin-induced hyperglycemia.

Authors:  S Ferber; A Halkin; H Cohen; I Ber; Y Einav; I Goldberg; I Barshack; R Seijffers; J Kopolovic; N Kaiser; A Karasik
Journal:  Nat Med       Date:  2000-05       Impact factor: 53.440

4.  Retinoic acid generated by Raldh2 in mesoderm is required for mouse dorsal endodermal pancreas development.

Authors:  Andrei Molotkov; Natalia Molotkova; Gregg Duester
Journal:  Dev Dyn       Date:  2005-04       Impact factor: 3.780

5.  NeuroD-betacellulin gene therapy induces islet neogenesis in the liver and reverses diabetes in mice.

Authors:  Hideto Kojima; Mineko Fujimiya; Kazuhiro Matsumura; Patrick Younan; Hirotsugu Imaeda; Makiko Maeda; Lawrence Chan
Journal:  Nat Med       Date:  2003-04-21       Impact factor: 53.440

6.  Notch signalling controls pancreatic cell differentiation.

Authors:  A Apelqvist; H Li; L Sommer; P Beatus; D J Anderson; T Honjo; M Hrabe de Angelis; U Lendahl; H Edlund
Journal:  Nature       Date:  1999-08-26       Impact factor: 49.962

Review 7.  Diabetes and hypertension: pathogenesis, prevention and treatment.

Authors:  Lewis Landsberg; Mark Molitch
Journal:  Clin Exp Hypertens       Date:  2004 Oct-Nov       Impact factor: 1.749

8.  Pancreatic polypeptide reduces appetite and food intake in humans.

Authors:  R L Batterham; C W Le Roux; M A Cohen; A J Park; S M Ellis; M Patterson; G S Frost; M A Ghatei; S R Bloom
Journal:  J Clin Endocrinol Metab       Date:  2003-08       Impact factor: 5.958

9.  SB-431542 is a potent and specific inhibitor of transforming growth factor-beta superfamily type I activin receptor-like kinase (ALK) receptors ALK4, ALK5, and ALK7.

Authors:  Gareth J Inman; Francisco J Nicolás; James F Callahan; John D Harling; Laramie M Gaster; Alastair D Reith; Nicholas J Laping; Caroline S Hill
Journal:  Mol Pharmacol       Date:  2002-07       Impact factor: 4.436

10.  Adult insulin- and glucagon-producing cells differentiate from two independent cell lineages.

Authors:  P L Herrera
Journal:  Development       Date:  2000-06       Impact factor: 6.868

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