scholarly journals Stress-induced adaptive islet cell identity changes

2016 ◽  
Vol 18 ◽  
pp. 87-96 ◽  
Author(s):  
V. Cigliola ◽  
F. Thorel ◽  
S. Chera ◽  
P. L. Herrera
Keyword(s):  
Islet Cell ◽  
Cell Identity ◽  
Identity Changes

scholarly journals Cellular plasticity at the nexus of development and disease

Development ◽  
2021 ◽  
Vol 148 (3) ◽  
pp. dev197392
Author(s):  
Lillian B. Spatz ◽  
Ramon U. Jin ◽  
Jason C. Mills
Keyword(s):  
Global Health ◽  
Initial Step ◽  
Cell Plasticity ◽  
Cell Identity ◽  
Fields Of Study ◽  
Poster Sessions ◽  
Epigenomic Regulation ◽  
Cellular Identity ◽  
Developmental Contexts ◽  
Identity Changes

ABSTRACTIn October 2020, the Keystone Symposia Global Health Series hosted a Keystone eSymposia entitled ‘Tissue Plasticity: Preservation and Alteration of Cellular Identity’. The event synthesized groundbreaking research from unusually diverse fields of study, presented in various formats, including live and virtual talks, panel discussions and interactive e-poster sessions. The meeting focused on cell identity changes and plasticity in multiple tissues, species and developmental contexts, both in homeostasis and during injury. Here, we review the key themes of the meeting: (1) cell-extrinsic drivers of plasticity; (2) epigenomic regulation of cell plasticity; and (3) conserved mechanisms governing plasticity. A salient take-home conclusion was that there may be conserved mechanisms used by cells to execute plasticity, with autodegradative activity (autophagy and lysosomes) playing a crucial initial step in diverse organs and organisms.

scholarly journals PAX6 maintains β cell identity by repressing genes of alternative islet cell types

2016 ◽  
Vol 127 (1) ◽  
pp. 230-243 ◽  
Author(s):  
Avital Swisa ◽  
Dana Avrahami ◽  
Noa Eden ◽  
Jia Zhang ◽  
Eseye Feleke ◽  
...  
Keyword(s):  
Islet Cell ◽  
Cell Types ◽  
Β Cell ◽  
Cell Identity ◽  
Islet Cell Types

scholarly journals Beta cell identity changes with mild hyperglycemia: Implications for function, growth, and vulnerability

2020 ◽  
Vol 35 ◽  
pp. 100959 ◽  
Author(s):  
Aref G. Ebrahimi ◽  
Jennifer Hollister-Lock ◽  
Brooke A. Sullivan ◽  
Ryohei Tsuchida ◽  
Susan Bonner-Weir ◽  
...  
Keyword(s):  
Beta Cell ◽  
Cell Identity ◽  
Mild Hyperglycemia ◽  
Identity Changes

scholarly journals Changes to the identity of EndoC-βH1 beta cells may be mediated by stress-induced depletion of HNRNPD

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Nicola Jeffery ◽  
David Chambers ◽  
Brandon M. Invergo ◽  
Ryan M. Ames ◽  
Lorna W. Harries
Keyword(s):  
Beta Cell ◽  
Beta Cells ◽  
Cell Population ◽  
Rna Binding ◽  
Rna Binding Proteins ◽  
Potential Candidate ◽  
Cell Identity ◽  
Patients With Diabetes ◽  
Stressed Cells ◽  
Identity Changes

Abstract Background Beta cell identity changes occur in the islets of donors with diabetes, but the molecular basis of this remains unclear. Protecting residual functional beta cells from cell identity changes may be beneficial for patients with diabetes. Results A somatostatin-positive cell population was induced in stressed clonal human EndoC-βH1 beta cells and was isolated using FACS. A transcriptomic characterisation of somatostatin-positive cells was then carried out. Gain of somatostatin-positivity was associated with marked dysregulation of the non-coding genome. Very few coding genes were differentially expressed. Potential candidate effector genes were assessed by targeted gene knockdown. Targeted knockdown of the HNRNPD gene induced the emergence of a somatostatin-positive cell population in clonal EndoC-βH1 beta cells comparable with that we have previously reported in stressed cells. Conclusions We report here a role for the HNRNPD gene in determination of beta cell identity in response to cellular stress. These findings widen our understanding of the role of RNA binding proteins and RNA biology in determining cell identity and may be important for protecting remaining beta cell reserve in diabetes.

scholarly journals Chronically Elevated Exogenous Glucose Elicits Antipodal Effects on the Proteome Signature of Differentiating Human iPSC-Derived Pancreatic Progenitors

2021 ◽  
Vol 22 (7) ◽  
pp. 3698
Author(s):  
Luiza Ghila ◽  
Thomas Aga Legøy ◽  
Andreas Frøslev Mathisen ◽  
Shadab Abadpour ◽  
Joao A. Paulo ◽  
...  
Keyword(s):  
Redox Balance ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Cell Identity ◽  
Glucose Levels ◽  
Pancreatic Progenitors ◽  
Exogenous Glucose ◽  
Extracellular Glucose ◽  
Identity Changes

The past decade revealed that cell identity changes, such as dedifferentiation or transdifferentiation, accompany the insulin-producing β-cell decay in most diabetes conditions. Mapping and controlling the mechanisms governing these processes is, thus, extremely valuable for managing the disease progression. Extracellular glucose is known to influence cell identity by impacting the redox balance. Here, we use global proteomics and pathway analysis to map the response of differentiating human pancreatic progenitors to chronically increased in vitro glucose levels. We show that exogenous high glucose levels impact different protein subsets in a concentration-dependent manner. In contrast, regardless of concentration, glucose elicits an antipodal effect on the proteome landscape, inducing both beneficial and detrimental changes in regard to achieving the desired islet cell fingerprint. Furthermore, we identified that only a subgroup of these effects and pathways are regulated by changes in redox balance. Our study highlights a complex effect of exogenous glucose on differentiating pancreas progenitors characterized by a distinct proteome signature.

Ulcerogenic Tumors of the Pancreas

1968 ◽  
Vol 26 ◽  
pp. 186-187
Author(s):  
J. C. Garancis ◽  
J. F. Kuzma ◽  
S. D. Wilson ◽  
E. H. Ellison
Keyword(s):  
Endoplasmic Reticulum ◽  
Tumor Cells ◽  
Islet Cell ◽  
Disease Process ◽  
Central Core ◽  
Islet Cell Tumors ◽  
Opaque Zone ◽  
Granular Form ◽  
Zollinger Ellison Syndrome

It has been proposed that a gastrin-like hormone elaborated by non-beta islet tumors of the pancreas may be responsible for a fulminating ulcer diathesis. Subsequently, a potent gastric secretagogue was isolated from ulcerogenic tumors of the pancreas. This disease process is known now as “Zollinger-Ellison syndrome”.In our studies of two cases of Zollinger-Ellison syndrome, pancreatic lesions were identified as alpha islet cell tumors (Fig. 1). Tumor cells were fairly uniform. The sizes of the alpha granules were not significantly different, but their number and distribution varied greatly from one cell to another. Each granule consisted of a round, highly dense central core, separated from the limiting membrane by an opaque zone. The granular form of the endoplasmic reticulum was particularly prominent. Numerous mitochondria, round or elongated, were dispersed throughout the cytoplasm. Individual or clusters of lysosomes were observed in the majority of cells.

Islet Cell Transplant Frees Patient From Insulin

2005 ◽  
Vol 38 (6) ◽  
pp. 15
Author(s):  
MICHELE G. SULLIVAN
Keyword(s):  
Islet Cell ◽  
Cell Transplant

Fetuin-A impairs maturation of pig neonatal islet cell clusters

2018 ◽  
Author(s):  
F Gerst ◽  
AK Fritz ◽  
E Lorza Gil ◽  
E Wolf ◽  
HU Häring ◽  
...  
Keyword(s):  
Islet Cell ◽  
Fetuin A ◽  
Cell Clusters
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