TY - JOUR
T1 - Pancreatic Progenitors
T2 - There and Back Again
AU - Domínguez-Bendala, Juan
AU - Qadir, Mirza Muhammad Fahd
AU - Pastori, Ricardo Luis
N1 - Funding Information:
We thank Dagmar Klein and Silvia Álvarez-Cubela for their critical reading of our manuscript. The corresponding authors are funded by the Diabetes Research Institute Foundation (DRIF) , the Inserra family , the Fred and Mabel R. Parks Foundation , the Foundation for Diabetes Research , the Tonkinson Foundation , the Michael J. and Katherine E. Franco Foundation , the Frank Strick Foundation , Mildred Graff , and NIH grants 1R43DK105655-01 , 2R44DK105655-02 and 1U01DK120393-01 (Human Islet Research Consortium, HIRN). M.M.F.Q is funded by an International Fulbright predoctoral fellowship/grant administered by the Foreign Fulbright Scholarship Board and the International Institute of Education .
Publisher Copyright:
© 2018 Elsevier Ltd
Copyright:
Copyright 2019 Elsevier B.V., All rights reserved.
PY - 2019/1
Y1 - 2019/1
N2 - Adult pancreatic regeneration is one of the most contentious topics in modern biology. The long-held view that the islets of Langerhans can be replenished throughout adult life through the reactivation of ductal progenitor cells has been replaced over the past decade by the now prevailing notion that regeneration does not involve progenitors and occurs only through the duplication of pre-existing mature cells. Here we dissect the limitations of lineage tracing (LT) to draw categorical conclusions about pancreatic regeneration, especially in view of emerging evidence that traditional lineages are less homogeneous and cell fates more dynamic than previously thought. This new evidence further suggests that the two competing hypotheses about regeneration are not mutually exclusive.
AB - Adult pancreatic regeneration is one of the most contentious topics in modern biology. The long-held view that the islets of Langerhans can be replenished throughout adult life through the reactivation of ductal progenitor cells has been replaced over the past decade by the now prevailing notion that regeneration does not involve progenitors and occurs only through the duplication of pre-existing mature cells. Here we dissect the limitations of lineage tracing (LT) to draw categorical conclusions about pancreatic regeneration, especially in view of emerging evidence that traditional lineages are less homogeneous and cell fates more dynamic than previously thought. This new evidence further suggests that the two competing hypotheses about regeneration are not mutually exclusive.
KW - dedifferentiation
KW - ductal cells
KW - human pancreatic progenitor cells
KW - islet regeneration
KW - type 1 diabetes
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U2 - 10.1016/j.tem.2018.10.002
DO - 10.1016/j.tem.2018.10.002
M3 - Review article
C2 - 30502039
AN - SCOPUS:85057285396
VL - 30
SP - 4
EP - 11
JO - Trends in Endocrinology and Metabolism
JF - Trends in Endocrinology and Metabolism
SN - 1043-2760
IS - 1
ER -
