Nestin-lineage cells contribute to the microvasculature but not endocrine cells of the islet

Mary Kay Treutelaar, Jennifer M. Skidmore, Claudia L. Dias-Leme, Manami Hara, Lizhi Zhang, Diane Simeone, Donna M. Martin, Charles F. Burant

Research output: Contribution to journalArticlepeer-review

128 Scopus citations

Abstract

To clarify the lineage relationship between cells that express the neural stem cell marker nestin and endocrine cells of the pancreas, we analyzed offspring of a cross between mice carrying a nestin promoter/enhancer-driven cre-recombinase (Nestin-cre) and C57BL/6J-Gtrosa26tm1Sor mice that carry a loxP-disrupted β-galactosidase gene (Rosa26). In nestin-cre +/tg;R26RloxP/+ embryos, cre-recombinase was detected in association with nestin-positive cells in the pancreatic mesenchyme with some of the nestin-positive cells lining vascular channels. In postnatal mice, pancreatic β-galactosidase expression was restricted to vascular endothelial cells of the islet and a subset of cells in the muscularis of arteries in a distribution identical to endogenous nestin expression. Ex vivo explants of mouse pancreatic ducts grew dense cultures that costained for nestin and β-galactosidase, demonstrating recombination in vitro. The cultures could be differentiated into complex stereotypic structures that contain nestin- and insulin-expressing cells. Nestin-cre+/tg; R26RloxP/+-derived duct cultures showed that insulin-positive cells were negative for β-galactosidase. These results indicate that both in vivo and in vitro pancreatic endocrine cells arise independently of nestin-positive precursors. The apparent vascular nature of the nestin-positive cell population and the close association with endocrine cells suggest that nestin-positive cells play an important role in the growth and maintenance of the islet.

Original languageEnglish (US)
Pages (from-to)2503-2512
Number of pages10
JournalDiabetes
Volume52
Issue number10
DOIs
StatePublished - Oct 1 2003

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism

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