Upregulation of nicotinic acetylcholine receptors in pulmonary arterial hypertension

Abstract

Smoking causes hypoxic vasospasm, thickening, and inflammation. Such responses are similar to the pathological mechanism of pulmonary arterial hypertension (PAH). PAH is a progressive and fatal disease that is characterized by the irreversible remodeling of the pulmonary artery. Pulmonary vasospasm, thickening, and inflammation are triggered by a chronic increase in cytosolic Ca 2+ concentration. Here, we focused on the expression of nicotinic acetylcholine receptors (nAChRs), which are associated with cytosolic Ca 2+ signaling, in PAH and hypoxic stress. The expression of the α subunits of nAChRs in pulmonary arterial smooth muscle cells (PASMCs) from normal subjects and idiopathic pulmonary arterial hypertension (IPAH) patients was analyzed by RT-PCR. Normal-PASMCs expressed nAChRα5 and α9 subunits. On the other hand, IPAH-PASMCs expressed nAChRα1, α5, and α7 subunits. As a result of Western blotting, the expression of nAChRα1and α7 proteins was upregulated in IPAH-PASMCs. In addition, the expression of nAChRα1 subunits was also increased in PASMCs from monocrotalineinduced pulmonary hypertensive rats. Furthermore, hypoxic exposure (1% O 2 ) increased nAChRα7 expression in normal-PASMCs. In conclusion, the expression of nAChRα1 and α7 subunits is upregulated in chronic respiratory diseases including PAH and hypoxic stress.

Activity Report on Information-Gathering of Database Literatures for Molten Salts

“…The books and literatures summarizing the handling and various experimental methods of molten salts are listed in Table 2. [19][20][21][22][23][24][25][26][27][28][29][30][31][32][33][34] "Molten Salt Techniques" published in the 1980s summarize the experimental techniques used in the early days of molten salt research. [20][21][22][23] For example, research on thermophysical properties was active at that time, but rare earth halide salts were available only as hydrates.…”