Adult pancreatic beta-cells are formed by self-duplication rather than stem-cell differentiation.
By Yuval Dor, Juliana R. Brown, O. I. Martinez, D. Melton. Nature, 2004
1,190 citations recorded by the source corpus.
View Paper: https://www.semanticscholar.org/paper/7830cd7b80f68bc0349f26d98bd3dc3aecaecea1
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Citations in the corpus
- Beta Cell Dysfunction and Insulin Resistance (2013, background): “Beta cell number increases markedly in the first year of rodent life (Montanya et al., 2000; Dor et al., 2004), up to 1.”
- Unlimited in vitro expansion of adult bi-potent pancreas progenitors through the Lgr5/R-spondin axis (2013, unknown): “Lineage tracing studies have demonstrated that these ‘ de novo beta cells’ can be derived from pre-existing beta cells (Dor et al , 2004), or by conversion of alpha cells, after almost 90% beta-cell ablation (Thorel et al , 2010).”
- Endogenous Bone Marrow MSCs Are Dynamic, Fate-Restricted Participants in Bone Maintenance and Regeneration (2012, background): “Cell replacement under homeostatic conditions or after injury is controlled either by symmetric division of existing mature cells (Dor et al., 2004) or by differentiation of stem/progenitor cells (Li and Clevers, 2010).”
- Evidence from a genetic fate-mapping study that stem cells refresh adult mammalian cardiomyocytes after injury (2007, methodology): “This 'pulse-chase' strategy has been used to study pancreatic beta-cell turnover in adult mice using an inducible Cre- loxP syste”
- β Cells Can Be Generated from Endogenous Progenitors in Injured Adult Mouse Pancreas (2008, background): “Both processes may be important in signaling for increase of the b cell mass under these conditions of injury, but it is unclear at this moment whether they play a role in the normal physiology of a healthy pancreas where the importance of self-duplication rather than stem cell differentiation is we”
- Stem cell plasticity: time for a reappraisal? (2005, unknown): “Moreover, recent data demonstrate that adult pancreatic insulin-producing cells are capable of replicating themselves.(27) However, the presence of additional sources of pancreatic precursor cells”
- Loss of autophagy diminishes pancreatic beta cell mass and function with resultant hyperglycemia. (2008, background): “We also studied whether autophagy is involved in b cell proliferation that occurs at a low level but is important for the maintenance of b cell mass (Dor et al., 2004).”
- Epigenetic reprogramming and induced pluripotency (2009, background): “…easily reprogrammed than lymphocytes because the pancreas is not organized into a hierarchical structure, as the hematopoietic system is (which contains stem, progenitor and differentiated cells) (Orkin and Zon, 2008), but rather reproduces its β cell pool by self duplication (Dor et al., 2004).”
- Growth and regeneration of adult beta cells does not involve specialized progenitors. (2007, background): “More recently, Melton and colleagues have employed insulinpromoter-based lineage tracing to suggest that adult b cells are the products of self-duplication (Dor et al., 2004).”
- Neuregulin1/ErbB4 signaling induces cardiomyocyte proliferation and repair of heart injury. (2009, unknown): “Examples of differentiated cells contributing to tissue renewal are insulin-producing b cells in the mouse pancreas (Dor et al., 2004), heart muscle cells in regenerating zebrafish hearts (Poss et al., 2002), tracheal cells in Drosophila larvae during metamorphosis (Guha et al., 2008; Weaver and…”
- Spinal Cord Injury Reveals Multilineage Differentiation of Ependymal Cells (2008, background): “Whether a specific cell population is derived from another cell type or it is maintained through self-duplication can be established by analyzing the genetic labeling frequency at different time points after induction of recombination [29,30].”
- Pancreas organogenesis: From bud to plexus to gland (2011, background): “…incorporation-based lineage tracing studies, under partial pancreatectomy (Ppx) conditions, have demonstrated that duplication of pre-existing b-cells represents a predominant mechanism of generating new b-cells in normal pancreas and under injury response (Dor et al., 2004; Teta et al., 2007).”