書誌事項
- タイトル別名
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- Upregulation of nicotinic acetylcholine receptors in pulmonary arterial hypertension
抄録
<p>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 Ca2+ concentration. Here, we focused on the expression of nicotinic acetylcholine receptors (nAChRs), which are associated with cytosolic Ca2+ 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 monocrotaline-induced pulmonary hypertensive rats. Furthermore, hypoxic exposure (1% O2) 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.</p>
収録刊行物
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- 日本薬理学会年会要旨集
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日本薬理学会年会要旨集 96 (0), 2-B-P-096-, 2022
公益社団法人 日本薬理学会
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詳細情報 詳細情報について
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- CRID
- 1390576037462402176
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- ISSN
- 24354953
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- 本文言語コード
- ja
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- データソース種別
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- JaLC
- Crossref
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- 抄録ライセンスフラグ
- 使用不可