Functional expression of cystic fibrosis transmembrane conductance regulator in mouse chondrocytes

Abstract

1. Cystic fibrosis transmembrane conductance regulator (CFTR) is well known for its role in the cystic fibrosis (CF). Recent studies have shown that CF patients and CFTR-deficient mice exhibit a severe abnormal skeletal phenotype, indicating that CFTR may play a role in bone development and pathophysiological processes. However, it is not known whether CFTR has a direct or indirect effect on bone formation. The aim of the present study was to detect the expression and function of CFTR in mouse chondrocytes. 2. Reverse transcription-polymerase chain reaction, western blotting and immunofluorescence were used to characterize the expression of CFTR in primary isolated mouse chondrocytes. Expression of CFTR mRNA and protein was detectable in mouse chondrocytes. Importantly, whole-cell patch-clamp analysis demonstrated that CFTR in mouse chondrocytes is functional as a cAMP-dependent Cl(-) channel that is inhibited by CFTRinh-172. 3. Thus, the results of the present study demonstrate that functional CFTR is expressed in mouse chondrocytes, which offers essential evidence for the potential direct role of CFTR in physiological and pathological processes of bone.