The role of nitric oxide in prostaglandin production by human pulmonary artery smooth muscle and endothelial cells.

一氧化氮在人肺动脉平滑肌和内皮细胞产生前列腺素中的作用。

• 批准号: 11670602
• 负责人: WATANABA Kentaro
• 金额: $ 2.18万
• 依托单位: Fukuoka University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 1999
• 资助国家: 日本
• 起止时间: 1999 至 2001
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-11670602/
• 关键词: human pulmonary artery smooty muscle cells; prostacyclin (pg12); nitric oxide (NO, nitrogen monooxide); cytokines; LIPOPOLYSACCHARIDE (LPS); COX-2s; NO合成酵素; 血管内細胞; プロスタグランディン; 肺動脈平滑筋細胞; Nitric oxide(NO); Prostacyclin(PGI_2); NO合成酵素(NOS)

Human pulmonary artery smooth muscle cells (HPASMC) were isolated and cultured from autopsy materials, and the effect of sodium nitroprusside (SNP) on cytokine- or lipopolysaccharide (LPS)-induced PGI2 production and expression of COX-2 antigen by HPASMC were examined to elucidate the relationship of the production of NO and prostaglandins by HPASMC. Eicosanoid profile by LPS-stimulated human umbilical vein endothelial ceUs(HUVEC) was also examined by HPLC.1) The enhanced production of PGI2 by LPS- and IL-1β-treated HPASMC was further augmented when HPASMC were treated with LPS or EL-1βtogether with SNP.2) In HUVEC, LPS enhanced the production of cyclooxygenase derivatives, but did not clearly enhance the production of lipoxygenase products. In contrasts, LPS enhanced the production of both cyclooxygenae and lipoxygenase products in HPASMC.3) Western blot analysis revealed that IL-1βaugmented the expression of COX-2 protein in HPASMC,From these experimental findings, it is suggested that1) NO enhances PGI2 production by HPASMC through the increased expression of COX-2 antigen.2) Pulmonary artery smooth muscle cells as well as endothelial cells could actively participate in the regulation of pulmonary blood flow and tonus of pulmonary artery by the interaction of NO and prostaglandins.

从尸检材料中分离培养人肺动脉平滑肌细胞（HPASMC），并检测硝普钠（SNP）对细胞因子或脂多糖（LPS）诱导的HPASMC产生PGI2和COX-2抗原表达的影响，以阐明HPASMC产生NO和前列腺素的关系。还通过 HPLC 检查了 LPS 刺激的人脐静脉内皮细胞 (HUVEC) 的类二十烷酸谱。1) 当用 LPS 或 EL-1β 与 SNP 一起处理 HPASMC 时，LPS 和 IL-1β 处理的 HPASMC 产生的 PGI2 增强进一步增强。2) 在 HUVEC 中，LPS 增强了环氧合酶的产生 衍生物，但没有明显增强脂氧合酶产物的产生。相比之下，LPS 增强了 HPASMC 中环氧合酶和脂氧合酶产物的产生。 3) Western blot 分析显示，IL-1β 增强了 HPASMC 中 COX-2 蛋白的表达。从这些实验结果来看，表明 1) NO 通过增加 COX-2 抗原的表达来增强 HPASMC 中 PGI2 的产生。 2) 肺动脉平滑肌细胞以及 内皮细胞可以通过NO与前列腺素的相互作用积极参与肺血流量和肺动脉张力的调节。

项目成果

FQ Wen, K Watanabe, M Yoshida: "Nitric oxide enhances PGI2 production by human pulmonary artery smooth muscle cells"Prostaglandins, Leukotrienes and Essential Fatty Acids. 62(6). 369-378 (2000)

FQ Wen、K Watanabe、M Yoshida：“一氧化氮增强人肺动脉平滑肌细胞的 PGI2 生成”前列腺素、白三烯和必需脂肪酸。

N Takahashi, T Iwanaga, K Watanabe 他: "Acute interstitial pneumonia induced by ONO-1078 (pranlukast), a leukotriene receptor antagonist"Internal Medicine. 40(8). 791-794 (2001)

N Takahashi、T Iwanaga、K Watanabe 等人：“白三烯受体拮抗剂 ONO-1078（普仑司特）诱导的急性间质性肺炎”，Internal Medicine 40(8) (2001)。

Watanabe Kentaro, Senju Shoji, Maeda Fumihiko, Yoshida Minoru: "Four cases of bronchiolitis obliterans organizing pneumonia associated with thyroid diseases"Respiration. 67. 572-576 (2000)

渡边健太郎、千手庄司、前田文彦、吉田稔：“甲状腺疾病相关闭塞性细支气管炎组织性肺炎四例”呼吸。

K Watanabe,S Senju,M Yosida 他: "Four cases of bronchiolitis obliterans organizing pneumonia associated with thyroid disease"Respiration. 67. 572-576 (2000)

K Watanabe、S Senju、M Yosida 等：“四例闭塞性细支气管炎组织性肺炎与甲状腺疾病相关”呼吸 67. 572-576 (2000)。

N.Tamaru, K.Watanabe, M.Yoshida, et al.: "Angiotensin-converting enzyme activity by canine pulmonary : microvascular and central pulmonary artery endothelial cells exposedto hypoxia"Lung. 178. 249-255 (2000)

N.Tamaru、K.Watanabe、M.Yoshida 等人：“犬肺血管紧张素转换酶活性：暴露于缺氧的微血管和中央肺动脉内皮细胞”肺。