Effect of Chronic Exposure to Cigarette Smoke on Canonical Transient Receptor Potential Expression in Rat Pulmonary Arterial Smooth Muscle.

In this study, we demonstrated that chronic cigarette smoke (CS) exposure leads to rat weight loss, right ventricular hypertrophy, and pulmonary artery remodeling. A fluorescence microscope was used to measure intracellular calcium concentration ([Ca(2+)]i) in rat distal PASMCs. Results showed that basal [Ca(2+)]i and store-operated calcium entry (SOCE) level in PASMCs from 3 and 6 months CS exposed rats were higher than those in the unexposed control group, among which the increase in 6 months CS group was more significant than that in 3 months group. Furthermore, chronic exposure to CS also increased TRPC1 and TRPC6 expression in both mRNA and protein levels. Simultaneously, in vitro study showed that nicotine treatment (10 nM) significantly increased basal [Ca(2+)]i and SOCE in cultured rat distal PASMCs, accompanied with upregulated TRPC1 and TRPC6 expression. Knochdown of TRPCs with specific siRNA indicated nicotine increased basal [Ca(2+)]i and SOCE in PASMC is TRPCs dependent. These results suggested that chronic cigarette smoking induced vascular tone changes in pulmonary arteries and the development of pulmonary hypertension might largely relate to the enhanced Ca(2+) entry and upregulation of TRPC1 and TRPC6 in PASMCs, in which nicotine played an indispensable role. PMID: 24336649 [PubMed - as supplied by publisher]
Source: American Journal of Physiology. Cell Physiology - Category: Cytology Authors: Tags: Am J Physiol Cell Physiol Source Type: research