Coupling Factor 6 Is Upregulated in Monocrotaline-Induced Pulmonary Arterial Hypertension Rats

Abstract Background Pulmonary arterial hypertension (PAH) is a rare and fatal disease. The prostacyclin (PGI2 ) pathway is a well-known therapeutic target for PAH. As a novel vasoconstrictive peptide, coupling factor 6 (CF6) has been recognized as the only endogenous inhibitor of PGI2 . However, the...

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Veröffentlicht in:The American journal of the medical sciences 2016-12, Vol.352 (6), p.631-636
Hauptverfasser: Li, Nannan, M.A, Yin, Jie, Ph.D, Cai, Weidong, Ph.D, Liu, Jingjing, Ph.D, Zhang, Na, Ph.D, Yan, Suhua, Ph.D, Song, Lucheng, Ph.D, Li, Xiaolu, Ph.D
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Sprache:eng
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Zusammenfassung:Abstract Background Pulmonary arterial hypertension (PAH) is a rare and fatal disease. The prostacyclin (PGI2 ) pathway is a well-known therapeutic target for PAH. As a novel vasoconstrictive peptide, coupling factor 6 (CF6) has been recognized as the only endogenous inhibitor of PGI2 . However, the relationship between CF6 and PAH is still unknown. Objective In this study, we investigated the involvement of CF6 in PAH in rats. Methods and results A total of 80 Sprague-Dawley rats were randomly divided into two groups: a control group (with saline intraperitoneally) and a monocrotaline (MCT)-treated group (with MCT 60mg/kg ip). The expression level of CF6 was measured by Immunohistochemistry, RT-PCR, and ELISA. The plasma level of 6-keto-PGF1α , a stable metabolite of PGI2 , was measured by ELISA. After MCT injection, while the plasma level of CF6 was markedly increased in a time-dependent manner, the level of 6-keto-PGF1α was decreased in the MCT rats as compared to that in the controls ( P
ISSN:0002-9629
1538-2990
DOI:10.1016/j.amjms.2016.08.002