|Cancer||Cell death||Cell cycle||Cytoskeleton||Exo/endocytosis||Differentiation||Division||Organelles||Signalling||Stem cells||Trafficking|
Cell Biology International (2011) 35, 463466 (Printed in Great Britain)
MicroRNAs and cystic fibrosis – an epigenetic perspective
Wenming Xu*†, Chen Hui†, Sidney Siu Bun Yu†, Chen Jing† and Hsiao Chang Chan*†1
*SCUCUHK Joint Laboratory for Reproductive Medicine, Institute of Women and Childrens Health, West China Second University Hospital, Sichuan University, Chengdu 610041, Peoples Republic of China, and †Epithelial Cell Biology Research Center, School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Shatin, NT, Hong Kong
CF (cystic fibrosis) is a recessive genetic disease caused by mutations of the CFTR (cystic fibrosis transmembrane conductance regulator), a cAMP-activated anion channel, exhibiting a multitude of clinical manifestations including lung inflammation/infection, pancreatic insufficiency/diabetes, intestinal obstruction and infertility in both sexes. While mutation DF508 is found in 70% of CF patients, large variation in disease phenotypes and severity is observed among the patients. This review discusses current theories accounting for the disease variations and puts forth an epigenetic hypothesis involving microRNAs.
Key words: CFTR, cystic fibrosis, epigenetic, microRNA
Abbreviations: CBAVD, bilateral absence of the vas deferens, CF, cystic fibrosis, CFTR, cystic fibrosis transmembrane conductance regulator; NF-κB, nuclear factor κB
1To whom correspondence should be addressed (email firstname.lastname@example.org).
Received 6 October 2010/1 December 2010; accepted 13 December 2010
Published online 30 March 2011, doi:10.1042/CBI20100664
© The Author(s) Journal compilation © 2011 Portland Press Limited