scholarly journals β-cell replacement sources for type 1 diabetes: a focus on pancreatic ductal cells

2016 ◽  
Vol 7 (4) ◽  
pp. 182-199 ◽  
Author(s):  
Elisa Corritore ◽  
Yong-Syu Lee ◽  
Etienne M. Sokal ◽  
Philippe A. Lysy
2016 ◽  
Vol 5 (10) ◽  
pp. 1338-1344 ◽  
Author(s):  
Daniel Pipeleers ◽  
Thomas Robert ◽  
Ines De Mesmaeker ◽  
Zhidong Ling

2016 ◽  
Vol 18 ◽  
pp. 137-143 ◽  
Author(s):  
A. Vieira ◽  
M. Courtney ◽  
N. Druelle ◽  
F. Avolio ◽  
T. Napolitano ◽  
...  

2005 ◽  
Vol 34 (2) ◽  
pp. 367-376 ◽  
Author(s):  
E Anastasi ◽  
C Santangelo ◽  
A Bulotta ◽  
F Dotta ◽  
B Argenti ◽  
...  

The elucidation of mechanisms regulating the regeneration and survival of pancreatic beta cells has fundamental implications in the cell therapy of type 1 diabetes. The present study had the following three aims: 1. to investigate whether pancreatic ductal epithelial cells can be induced to differentiate into insulin-producing cells by exposing them to hepatocyte growth factor (HGF); 2. to characterize some of the molecular events leading to their differentiation toward a beta-cell-like phenotype; 3. to evaluate the susceptibility of newly differentiated insulin-secreting cells to cytokine-induced apoptosis, a mechanism of beta-cell destruction occurring in type 1 diabetes. We demonstrated that HGF-treated rat pancreatic ductal cell line (ARIP) cells acquired the capability to transcribe the insulin gene and translate its counterpart protein. HGF-treated cells also exhibited a glucose-dependent capability to secrete insulin into the cultured medium. Expression analysis of some of the genes regulating pancreatic beta-cell differentiation revealed a time-dependent transcription of neurogenin-3 and Neuro-D in response to HGF. Finally, we determined the susceptibility to proinflammatory cytokine (PTh1)-induced apoptosis by incubating HGF-treated and untreated ARIP cells with a cocktail of interleukin-1 beta (IL-1β), tumor necrosis factor-alpha (TNF-α) and interferon-gamma (IFN-γ). Such treatment induced apoptotic death, as determined by the TUNEL technique, in about 40% of HGF-treated, insulin-secreting ARIP cells, while untreated ARIP cells were resistant to PTh1-induced apoptosis. In conclusion, we showed that HGF promotes the differentiation of ARIP cells into pancreatic beta-cell-like cells, and that the differentiation toward an insulin-secreting phenotype is associated with the appearance of susceptibility to cytokine-induced apoptosis.


Diabetes ◽  
2014 ◽  
Vol 63 (5) ◽  
pp. 1433-1444 ◽  
Author(s):  
Giuseppe Orlando ◽  
Pierre Gianello ◽  
Marcus Salvatori ◽  
Robert J. Stratta ◽  
Shay Soker ◽  
...  

Nanomedicine ◽  
2020 ◽  
Vol 15 (18) ◽  
pp. 1735-1738
Author(s):  
Silke Krol ◽  
Walter Baronti ◽  
Piero Marchetti

Science ◽  
2021 ◽  
Vol 373 (6554) ◽  
pp. 516-522 ◽  
Author(s):  
Todd M. Brusko ◽  
Holger A. Russ ◽  
Cherie L. Stabler

Technological advancements in blood glucose monitoring and therapeutic insulin administration have improved the quality of life for people with type 1 diabetes. However, these efforts fall short of replicating the exquisite metabolic control provided by native islets. We examine the integrated advancements in islet cell replacement and immunomodulatory therapies that are coalescing to enable the restoration of endogenous glucose regulation. We highlight advances in stem cell biology and graft site design, which offer innovative sources of cellular material and improved engraftment. We also cover cutting-edge approaches for preventing allograft rejection and recurrent autoimmunity. These insights reflect a growing understanding of type 1 diabetes etiology, β cell biology, and biomaterial design, together highlighting therapeutic opportunities to durably replace the β cells destroyed in type 1 diabetes.


2020 ◽  
Vol 14 (1) ◽  
pp. 91-104 ◽  
Author(s):  
Aaron A. Stock ◽  
Vita Manzoli ◽  
Teresa De Toni ◽  
Maria M. Abreu ◽  
Yeh-Chuin Poh ◽  
...  

Author(s):  
Michelle J. Quizon ◽  
Andrés J. García

While significant progress has been made in treatments for type 1 diabetes (T1D) based on exogenous insulin, transplantation of insulin-producing cells (islets or stem cell–derived β cells) remains a promising curative strategy. The current paradigm for T1D cell therapy is clinical islet transplantation (CIT)—the infusion of islets into the liver—although this therapeutic modality comes with its own limitations that deteriorate islet health. Biomaterials can be leveraged to actively address the limitations of CIT, including undesired host inflammatory and immune responses, lack of vascularization, hypoxia, and the absence of native islet extracellular matrix cues. Moreover, in efforts toward a clinically translatable T1D cell therapy, much research now focuses on developing biomaterial platforms at the macroscale, at which implanted platforms can be easily retrieved and monitored. In this review, we discuss how biomaterials have recently been harnessed for macroscale T1D β cell replacement therapies. Expected final online publication date for the Annual Review of Pathology: Mechanisms of Disease, Volume 17 is January 2022. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.


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