Pulmonary Vascular Disease: Pulmonary Vascular Disease: PAH |

Effects of Chronic Exposure to Cigarette Smoke on Canonical Transient Receptor Potential Expression in Rat Pulmonary Arterial Smooth Muscle FREE TO VIEW

Ruimin Hu; Yuqin Chen; Dejun Sun; Jian Wang
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Inner Mongolia People’s Hospital, Huhhot, China

Copyright 2016, American College of Chest Physicians. All Rights Reserved.

Chest. 2016;149(4_S):A510. doi:10.1016/j.chest.2016.02.532
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SESSION TITLE: Pulmonary Vascular Disease: PAH

SESSION TYPE: Original Investigation Poster

PRESENTED ON: Saturday, April 16, 2016 at 11:45 AM - 12:45 PM

PURPOSE: To clarify the possible mechanism of chronic cigarette smoke (CS)-induced pulmonary hypertension and furthermore provide effective targets for prevention and treatment.

METHODS: The effects of chronic CS on rat pulmonary arterial smooth muscle in vivo and nicotine treatment on rat PASMCs in vitro were investigated. A fluorescence microscope was used to measure the basal intracellular calcium concentration ([Ca2+]i) and store operated calcium entry (SOCE) in rat PASMC; The expression of transient receptor potential 1 (TRPC1) and transient receptor potential 6 (TRPC6) at both mRNA and protein levels in isolated distal PA was examinated using Western blot and real-time PCR.

RESULTS: In this study, we demonstrated that chronic CS exposure led to rat weight loss, right ventricular hypertrophy, and pulmonary arterial remodeling. Results showed that basal [Ca2+]i and SOCE levels in PASMCs from 3-mo and 6-mo CS-exposed rats were markedly higher than those in cells from the unexposed control animals (the increases in 6-mo CS group were more significant than that in 3-mo CS group), accompanied with increased canonical TRPC1 and TRPC6 expression at both mRNA and protein levels in isolated distal PA. Simultaneously, in vitro study showed that nicotine treatment (10 nM) significantly increased the basal [Ca2+]i and SOCE and upregulated TRPC1 and TRPC6 expression at both mRNA and protein levels in cultured rat distal PASMCs. TRPC siRNA knockdown strategies revealed that the elevations of basal [Ca2+]i and SOCE induced by nicotine in PASMCs were TRPC1 and TRPC6 dependent.

CONCLUSIONS: These observations suggest that nicotine elevates [Ca2+]i via TRPCs which play an important role in occurring and developing of pulmonary hypertension in rat PASMCs, and demonstrate how nicotine affects the intracellular calcium homeostasis, and provide some suggestions of the diagnosis and treatment of nicotine induced PH.


DISCLOSURE: The following authors have nothing to disclose: Ruimin Hu, Yuqin Chen, Dejun Sun, Jian Wang

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