Title Information
Title
Transdifferentiation of liver to pancreas
Name: Personal
Name Part
Srivastava, Akash
Role
Role Term: Text
creator
Origin Information
Copyright Date
2015
Physical Description
Extent
15, 177 p.
digitalOrigin
born digital
Note
Thesis (Ph.D. -- Brown University (2015)
Name: Personal
Name Part
Horb, Marko
Role
Role Term: Text
Director
Name: Personal
Name Part
Freiman, Richard
Role
Role Term: Text
Reader
Name: Personal
Name Part
Morrow, Eric
Role
Role Term: Text
Reader
Name: Personal
Name Part
Wharton, Kristi
Role
Role Term: Text
Reader
Name: Personal
Name Part
Zorn, Aaron
Role
Role Term: Text
Reader
Name: Corporate
Name Part
Brown University. BIOMED: Molecular Biology, Cell Biology, and Biochemistry
Role
Role Term: Text
sponsor
Genre (aat)
theses
Abstract
Diabetes mellitus results from gradual decline in pancreatic beta cell mass and function. Cell-based therapies in diabetes research are mainly focused on using stem cells to produce pancreatic beta cells in vitro for transplantation. A promising alternative strategy is to generate pancreatic tissue from other tissues already present in the body by transdifferentiation. Liver provides the best alternative source of tissue to create ectopic pancreatic tissue because liver has the highest regenerative capacity among all parenchymal organs and only few key developmental steps specify liver and pancreatic lineages during organogenesis. To this end, transdifferentiation of liver to pancreas has been reported in different systems but the molecular mechanism of this process is currently unknown. Using transgenic Xenopus tadpoles we previously showed that Pdx1-VP16 converts liver cells into all pancreatic cell types (both endocrine and exocrine), while Ptf1a-VP16 converts liver cells to only acinar (exocrine) cells. However, which genes are activated by Pdx1-VP16 or Ptf1a-VP16 in this process is unknown. In order to gain insight into the gene regulatory networks controlled by Pdx1-VP16 and Ptf1a-VP16 during the transdifferentiation of liver to pancreas, we performed a microarray analysis and compared the gene expression profile of transgenic tadpoles with that of control tadpoles. We found upregulation of β-catenin inhibitor Chibby homolog1 (Cby) in Ptf1a-VP16 microarray. We demonstrated that cby is expressed in transdifferentiated livers of Ptf1aVP16 transgenic tadpoles and also in developing foregut organs (stomach/duodenum and pancreas) in wild-type Xenopus embryos. By overexpressing cby in Xenopus transgenic tadpole livers at NF 44-45, we demonstrated that expression of cby converts tadpole liver to ectopic endocrine pancreas, whereas using gain-of-function and loss-of-function experiments in early endoderm of wild-type Xenopus embryos we showed that cby promotes the formation of exocrine pancreas during normal pancreas development. Further analyses of these phenotypes indicated that inhibition of β-catenin might have two different roles in early versus late pancreas development. A better understanding of the molecular mechanism involved in transdifferentiation of liver to pancreas would enable researchers to create functional pancreatic beta cells from liver cells for thetreatment of diabetes.
Subject
Topic
Transdifferentiation
Subject
Topic
Pdx1-VP16
Subject
Topic
Ptf1a-VP16
Subject
Topic
Chibby
Subject (FAST) (authorityURI="http://id.worldcat.org/fast", valueURI="http://id.worldcat.org/fast/1000617")
Topic
Liver
Subject (FAST) (authorityURI="http://id.worldcat.org/fast", valueURI="http://id.worldcat.org/fast/1051970")
Topic
Pancreas
Record Information
Record Content Source (marcorg)
RPB
Record Creation Date (encoding="iso8601")
20150601
Language
Language Term: Code (ISO639-2B)
eng
Language Term: Text
English
Identifier: DOI
10.7301/Z0Z60MF3
Access Condition: rights statement (href="http://rightsstatements.org/vocab/InC/1.0/")
In Copyright
Access Condition: restriction on access
Collection is open for research.
Type of Resource (primo)
dissertations