Patient-derived pancreas-on-a-chip to model cystic fibrosis-related disorders

Kyu Shik Mun, Kavisha Arora, Yunjie Huang, Fanmuyi Yang, Sunitha Yarlagadda, Yashaswini Ramananda, Maisam Abu-El-Haija, Joseph J. Palermo, Balamurugan N. Appakalai, Jaimie D. Nathan () and Anjaparavanda P. Naren ()
Additional contact information
Kyu Shik Mun: Cincinnati Children’s Hospital Medical Center
Kavisha Arora: Cincinnati Children’s Hospital Medical Center
Yunjie Huang: Cincinnati Children’s Hospital Medical Center
Fanmuyi Yang: Cincinnati Children’s Hospital Medical Center
Sunitha Yarlagadda: Cincinnati Children’s Hospital Medical Center
Yashaswini Ramananda: Cincinnati Children’s Hospital Medical Center
Maisam Abu-El-Haija: Cincinnati Children’s Hospital Medical Center
Joseph J. Palermo: Cincinnati Children’s Hospital Medical Center
Balamurugan N. Appakalai: University of Louisville
Jaimie D. Nathan: Cincinnati Children’s Hospital Medical Center
Anjaparavanda P. Naren: Cincinnati Children’s Hospital Medical Center

Nature Communications, 2019, vol. 10, issue 1, 1-12

Abstract: Abstract Cystic fibrosis (CF) is a genetic disorder caused by defective CF Transmembrane Conductance Regulator (CFTR) function. Insulin producing pancreatic islets are located in close proximity to the pancreatic duct and there is a possibility of impaired cell-cell signaling between pancreatic ductal epithelial cells (PDECs) and islet cells as causative in CF. To study this possibility, we present an in vitro co-culturing system, pancreas-on-a-chip. Furthermore, we present an efficient method to micro dissect patient-derived human pancreatic ducts from pancreatic remnant cell pellets, followed by the isolation of PDECs. Here we show that defective CFTR function in PDECs directly reduced insulin secretion in islet cells significantly. This uniquely developed pancreatic function monitoring tool will help to study CF-related disorders in vitro, as a system to monitor cell-cell functional interaction of PDECs and pancreatic islets, characterize appropriate therapeutic measures and further our understanding of pancreatic function.

Date: 2019
References: Add references at CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/s41467-019-11178-w Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:10:y:2019:i:1:d:10.1038_s41467-019-11178-w

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/s41467-019-11178-w

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().