Regulation of Pancreatic Islet Formation

Carrasco, Manuel; Rojas, Anabel; Delgado, Irene; Vuilleumier, Nadia Cobo; Tejedo, Juan R.; Bedoya, Francisco J.; Gauthier, Benoît; Soria, Bernat; Martı́n, Franz

doi:10.1007/978-94-007-6686-0_36

Cited by 4 publications

(2 citation statements)

References 117 publications

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“…Identifying factors or signals that regulate these processes that are potentially triggered and sustained by the autoimmune environment will be the key to harnessing a successful in vivo regenerative therapy. [182]. High expression levels of Pax4 relative to Arx were shown to favor a b-cell phenotype, whereas low levels relative to Arx result in an a-cell phenotype [67].…”

Section: Minimal Standards To Accept a B-cell Surrogatementioning

confidence: 97%

Using stem cells to produce insulin

Soria

Gauthier²,

Martı́n

et al. 2015

Expert Opinion on Biological Therapy

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Section: Minimal Standards To Accept a B-cell Surrogatementioning

confidence: 97%

Using stem cells to produce insulin

Soria

Gauthier²,

Martı́n

et al. 2015

Expert Opinion on Biological Therapy

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“…Pancreatic islets have complex structures formed from the embryonic endoderm in several steps (Carrasco et al, ). Pancreatic islet β‐cells are derived in the processes of specification, growth, and differentiation (Murtaugh, ).…”

Section: Mirnas In Islet β‐Cell Developmentmentioning

confidence: 99%

The role of microRNAs in islet β‐cell development

Kaviani

Azarpira

Karimi

et al. 2016

Cell Biology International

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Cell-based therapies suggest novel treatments to overcome the complication of the current therapeutic approaches in diabetes mellitus type 1. Replacement of the destroyed pancreatic islet β-cells by appropriate alternative cells needs an efficient approach to differentiate the cells into viable and functional insulin producing cells. Small non-coding RNA molecules, microRNAs (miRNA), have critical roles in post-transcriptional regulation of gene expression. Therefore, they can direct the cells toward β-cell like cells and control islet β-cell development. Previous reports showed the manipulation of the miRNA expression on islet β-cell differentiation and regeneration. Likewise, the regulation of epithelial to mesenchymal transi-tion by the miR-30 family and the miR-200 family may be a useful approach to conduct islet β-cell development. Investigation of stem cells differentiation showed that the dynamic expression patterns of miR-375 and miR-7 are similar to developing human fetal pancreas while dynamic expression of miR-146a and miR-34a occurred during the differentiation. Moreover, miR-342 and its both targets, FOXA2 and MAFB, are found in β-cell differentiation and maturation. Because miRNAs can target specific transcription factors during islet β-cell development and differentiation, they could be offerred as alternative regenerative treatment for diabetes mellitus. Considering that the application of these non-coding RNAs remains limited in the literature, in this review article, we present an overview of the roles of miRNAs in the islet β-cell development, focusing on the application of different miRNAs in the experimental protocols.

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PAX4 Defines an Expandable β-Cell Subpopulation in the Adult Pancreatic Islet

Lorenzo

Fuente-Martín

Brun

et al. 2015

Sci Rep

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PAX4 is a key regulator of pancreatic islet development whilst in adult acute overexpression protects β-cells against stress-induced apoptosis and stimulates proliferation. Nonetheless, sustained PAX4 expression promotes β-cell dedifferentiation and hyperglycemia, mimicking β-cell failure in diabetic patients. Herein, we study mechanisms that allow stringent PAX4 regulation endowing favorable β-cell adaptation in response to changing environment without loss of identity. To this end, PAX4 expression was monitored using a mouse bearing the enhanced green fluorescent protein (GFP) and cre recombinase construct under the control of the islet specific pax4 promoter. GFP was detected in 30% of islet cells predominantly composed of PAX4-enriched β-cells that responded to glucose-induced insulin secretion. Lineage tracing demonstrated that all islet cells were derived from PAX4+ progenitor cells but that GFP expression was confined to a subpopulation at birth which declined with age correlating with reduced replication. However, this GFP+ subpopulation expanded during pregnancy, a state of active β-cell replication. Accordingly, enhanced proliferation was exclusively detected in GFP+ cells consistent with cell cycle genes being stimulated in PAX4-overexpressing islets. Under stress conditions, GFP+ cells were more resistant to apoptosis than their GFP- counterparts. Our data suggest PAX4 defines an expandable β-cell sub population within adult islets.

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Regulation of Pancreatic Islet Formation

Cited by 4 publications

References 117 publications

Using stem cells to produce insulin

Using stem cells to produce insulin

The role of microRNAs in islet β‐cell development

PAX4 Defines an Expandable β-Cell Subpopulation in the Adult Pancreatic Islet

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