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Retinoic acid increases the length and volume density of ducts in the rat embryonic pancreas
Author(s) -
Erasmus Carene,
Penny Clem,
Kramer Beverly
Publication year - 2003
Publication title -
development, growth and differentiation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.864
H-Index - 66
eISSN - 1440-169X
pISSN - 0012-1592
DOI - 10.1034/j.1600-0854.2004.00685.x
Subject(s) - matrigel , glucagon , retinoic acid , insulin , medicine , bromodeoxyuridine , endocrinology , pancreas , biology , explant culture , embryonic stem cell , cell growth , immunocytochemistry , chemistry , cell , cell culture , in vitro , biochemistry , genetics , gene
In this study, the role of all ‐trans retinoic acid (RA) on the proliferation of rat embryonic pancreas ducts and on the proportion of insulin cells was investigated. All‐ trans RA (10 −6 m ) was added to Ham's F12.ITS serum‐free medium in which 12.5 day rat dorsal pancreatic buds were cultured on Matrigel. Control explants were cultured on Matrigel in Ham's F12.ITS alone or in Ham's F12.ITS containing ethanol (the diluent for RA). After a 7 day culture period, explants were incubated with bromodeoxyuridine (BrdU) for assessment of cell proliferation. Explants were processed for both morphometry and immunocytochemistry. The length density and volume density of the pancreatic ducts were assessed using an image analysis system. Cells positive for insulin, BrdU and glucagon were localized on adjacent serial sections. RA treatment caused a statistically significant increase in the volume density ( P < 0.007) and length density ( P < 0.008) of the ducts, as well as a 1.2‐fold increase ( P < 0.0001) in the proportion of insulin to glucagon cells, compared to both control groups. Few insulin cells were BrdU positive, indicating that cells had a low proliferation rate. The increased proportion of insulin cells may relate to the increased volume density and length density of the ducts in RA‐treated explants. It is suggested that RA stimulated the production of additional progenitor cells and not proliferation of existing insulin cells.