Document Detail


Remodeling of insulin producing beta-cells during Xenopus laevis metamorphosis.
MedLine Citation:
PMID:  19389350     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Insulin-producing beta-cells are present as single cells or in small clusters distributed throughout the pancreas of the Xenopus laevis tadpole. During metamorphic climax when the exocrine pancreas dedifferentiates to progenitor cells, the beta-cells undergo two changes. Insulin mRNA is down regulated at the beginning of metamorphic climax (NF62) and reexpressed again near the end of climax. Secondly, the beta-cells aggregate to form islets. During climax the increase in insulin cluster size is not caused by cell proliferation or by acinar-to-beta-cell transdifferentiation, but rather is due to the aggregation of pre-existing beta-cells. The total number of beta-cells does not change during the 8 days of climax. Thyroid hormone (TH) induction of premetamorphic tadpoles causes an increase in islet size while prolonged treatment of tadpoles with the goitrogen methimazole inhibits this increase. Expression of a dominant negative form of the thyroid hormone receptor (TRDN) driven by the elastase promoter not only protects the exocrine pancreas of a transgenic tadpole from TH-induced dedifferentiation but also prevents aggregation of beta-cells at climax. These transgenic tadpoles do however undergo normal loss and resynthesis of insulin mRNA at the same stage as controls. In contrast transgenic tadpoles with the same TRDN transgene driven by an insulin promoter do not undergo down regulation of insulin mRNA, but do aggregate beta-cells to form islets like controls. These results demonstrate that TH controls the remodeling of beta-cells through cell-cell interaction with dedifferentiating acinar cells and a cell autonomous program that temporarily shuts off the insulin gene.
Authors:
Sandeep Mukhi; Marko E Horb; Donald D Brown
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2009-02-04
Journal Detail:
Title:  Developmental biology     Volume:  328     ISSN:  1095-564X     ISO Abbreviation:  Dev. Biol.     Publication Date:  2009 Apr 
Date Detail:
Created Date:  2009-04-27     Completed Date:  2009-06-09     Revised Date:  2014-09-14    
Medline Journal Info:
Nlm Unique ID:  0372762     Medline TA:  Dev Biol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  384-91     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Animals, Genetically Modified
Cell Aggregation / drug effects,  physiology
Cell Differentiation / drug effects,  physiology
Gene Expression Regulation, Developmental
Insulin / biosynthesis*,  genetics
Insulin-Secreting Cells / cytology,  physiology
Islets of Langerhans / cytology,  growth & development,  physiology*
Metamorphosis, Biological / drug effects,  physiology*
RNA, Messenger / biosynthesis
Receptors, Thyroid Hormone / physiology
Thyroid Hormones / pharmacology,  physiology
Xenopus Proteins / genetics,  metabolism*
Xenopus laevis / growth & development,  physiology*
Grant Support
ID/Acronym/Agency:
DK077197/DK/NIDDK NIH HHS; R01 DK077197/DK/NIDDK NIH HHS; R01 DK077197-04/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Insulin; 0/RNA, Messenger; 0/Receptors, Thyroid Hormone; 0/Thyroid Hormones; 0/Xenopus Proteins
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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