PMID- 10792952
OWN - NLM
STAT- MEDLINE
DCOM- 20000614
LR  - 20151119
IS  - 0022-4804 (Print)
IS  - 0022-4804 (Linking)
VI  - 90
IP  - 2
DP  - 2000 May 15
TI  - In vitro validation of duct differentiation in developing embryonic mouse 
      pancreas.
PG  - 126-30
AB  - BACKGROUND: Early embryonic pancreatic epithelia have the capacity for either 
      endocrine or exocrine lineage commitment. Recent studies demonstrated the 
      pluripotential nature of these undifferentiated cells. Isolated pancreatic 
      epithelia grown under the renal capsule formed primarily islets. However, when 
      these same epithelia were grown in a basement-membrane-rich gel (Matrigel) they 
      formed mostly ducts. Currently, there is no model for in vitro pancreatic duct 
      formation and therefore, the mechanism of duct morphogenesis has never been 
      described. The purpose of this study was to provide such a model by 
      characterizing the expression of two duct markers, carbonic anhydrase II (CAII) 
      and the cystic fibrosis transmembrane conductance regulator (CFTR), in isolated 
      undifferentiated pancreatic epithelia grown in vitro. MATERIALS AND METHODS: We 
      microdissected embryonic pancreases at Embryonic Days (E)9.5-11.5 and performed 
      RT-PCR for CAII and CFTR on E9.5 whole pancreases, E10. 5 and E11.5 epithelia, as 
      well as E11.5 epithelia grown for 7 days in Matrigel. Next we performed in situ 
      hybridization for CAII and CFTR and immunohistochemistry for CAII on E11.5 
      epithelia grown for 7 days in Matrigel. RESULTS: Early, undifferentiated 
      embryonic pancreatic epithelium does not express CAII and CFTR by RT-PCR. When 
      E11.5 epithelia were grown for 7 days in Matrigel, however, gene expression for 
      both markers is upregulated as ducts form. Furthermore, CAII was seen by IHC and 
      both CAII and CFTR were seen by in situ hybridization in the ducts after 7 days 
      in Matrigel. CONCLUSIONS: These data validate our in vitro system as a model for 
      studying the mechanism of normal pancreatic duct differentiation and may 
      potentially help us to understand the faulty mechanism involved in pancreatic 
      ductal carcinogenesis.
CI  - Copyright 2000 Academic Press.
FAU - Kadison, A S
AU  - Kadison AS
AD  - New York University Medical Center, New York, New York, USA.
FAU - Maldonado, T S
AU  - Maldonado TS
FAU - Crisera, C A
AU  - Crisera CA
FAU - Longaker, M T
AU  - Longaker MT
FAU - Gittes, G K
AU  - Gittes GK
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Surg Res
JT  - The Journal of surgical research
JID - 0376340
RN  - 0 (Biomarkers)
RN  - 0 (RNA, Messenger)
RN  - 126880-72-6 (Cystic Fibrosis Transmembrane Conductance Regulator)
RN  - EC 4.2.1.1 (Carbonic Anhydrases)
SB  - IM
MH  - Animals
MH  - Biomarkers
MH  - Carbonic Anhydrases/genetics
MH  - Cell Culture Techniques/*methods/*standards
MH  - Cell Differentiation/physiology
MH  - Cystic Fibrosis Transmembrane Conductance Regulator/genetics
MH  - Epithelial Cells/chemistry/cytology/enzymology
MH  - Female
MH  - Gene Expression Regulation, Developmental
MH  - Gene Expression Regulation, Enzymologic
MH  - In Situ Hybridization
MH  - Mice
MH  - Mice, Inbred Strains
MH  - Pancreatic Ducts/*cytology/*embryology
MH  - Pregnancy
MH  - RNA, Messenger/analysis
MH  - Reproducibility of Results
MH  - Reverse Transcriptase Polymerase Chain Reaction
EDAT- 2000/05/04 09:00
MHDA- 2000/06/17 09:00
CRDT- 2000/05/04 09:00
PHST- 2000/05/04 09:00 [pubmed]
PHST- 2000/06/17 09:00 [medline]
PHST- 2000/05/04 09:00 [entrez]
AID - S0022-4804(00)95876-1 [pii]
AID - 10.1006/jsre.2000.5876 [doi]
PST - ppublish
SO  - J Surg Res. 2000 May 15;90(2):126-30. doi: 10.1006/jsre.2000.5876.