The mechanisms that restrict regeneration and maintain cell identity following injury are poorly characterized in higher vertebrates. Following β-cell loss, 1-2% of the glucagon-producing α-cells spontaneously engage in insulin production in mice. Here we explore the mechanisms inhibiting α-cell plasticity.…
Tag: publications
Research Paper: β-cell proteomic landscape in differentiating MODY1 patient iPSC-derived cells
Current published protocols for targeted differentiation of human stem cells toward pancreatic β-cells fail to deliver sufficiently mature cells with functional properties comparable to human islet β-cells. We aimed to assess whether Wnt-modulation could promote the final protocol stages of…
Collaboration Paper: Converting Adult Pancreatic Islet α Cells into β Cells by Dnmt1-Arx
Chakravarthy et al. dissect the mechanisms maintaining α cell identity and reveal that simultaneous inactivation of the DNA methyltransferase Dnmt1 and the transcription factor Arx in adult mice drives the conversion of α- to β-like cells. In human T1D islets, glucagon+ cells lose DNMT1 and ARX expression and express β cell markers.
Review: Stress-induced adaptive islet cell identity changes
Here, we discuss the latest findings on pancreas and islet cell plasticity upon physiological, pathological and experimental conditions of stress. Understanding the mechanisms involved in cell reprogramming will allow the development of new strategies for the treatment of diabetes, by exploiting the intrinsic regeneration capacity of the pancreas.
Review: in situ Regeneration of Pancreatic Insulin-Producing Cells
The prevalence of diabetes will rise from 2.8% of the total world population in 2000 to 4.4% in 2030. The two prevailing forms of diabetes, named Type 1 and Type 2 (T1D and T2D), are chronic and often lead to…