To continue reading this article, sign up for FREE to
Membership is FREE
and provides you with
instant access
to email newsletters, digital publications, our full content catalogue & more...
Already have an account?
Impaired Metabolism in Cystic Fibrosis Lung Epithelial Cells Revealed by Metabolic Analysis
Read time: Less than a minute
Metabolon, Inc., announces the publication of “Metabolomic Profiling Reveals Biochemical Pathways and Biomarkers Associated with Pathogenesis in Cystic Fibrosis Cells”, in the Journal of Biological Chemistry (2010, Vol. 285, No. 40, Pages 30516-30522). The article describes the application of non-targeted biochemical profiling (metabolomics) to study the biochemical changes in human lung epithelial cell lines of cystic fibrosis (CF) patients.
The study was carried out in collaboration with the Cystic Fibrosis Foundation Therapeutics, Inc. (CFFT), a nonprofit subsidiary of the Cystic Fibrosis Foundation, and CF researchers from the University of Pittsburgh funded by CFFT.
The identification of the cystic fibrosis transmembrane conductance regulator (CFTR) gene has lead to many genetic and molecular biology studies which have aided our understanding of the effects of gene mutations on the CFTR protein. Yet, how the CFTR defects lead to downstream biological changes and the resulting CF clinical symptoms remains unclear.
In the JBC report, the investigators used metabolomics to gain an initial understanding of the global biochemical alterations in CF primary lung epithelial cells. The authors measured changes in glucose, sorbitol and pentose phosphate metabolism that could serve to exacerbate CF-associated oxidative stress as well as other metabolic changes that suggest altered purinergic signaling.
The study was carried out in collaboration with the Cystic Fibrosis Foundation Therapeutics, Inc. (CFFT), a nonprofit subsidiary of the Cystic Fibrosis Foundation, and CF researchers from the University of Pittsburgh funded by CFFT.
The identification of the cystic fibrosis transmembrane conductance regulator (CFTR) gene has lead to many genetic and molecular biology studies which have aided our understanding of the effects of gene mutations on the CFTR protein. Yet, how the CFTR defects lead to downstream biological changes and the resulting CF clinical symptoms remains unclear.
In the JBC report, the investigators used metabolomics to gain an initial understanding of the global biochemical alterations in CF primary lung epithelial cells. The authors measured changes in glucose, sorbitol and pentose phosphate metabolism that could serve to exacerbate CF-associated oxidative stress as well as other metabolic changes that suggest altered purinergic signaling.
