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Caffeic Acid Phenethyl Ester Rescues Pulmonary Arterial Hypertension through the Inhibition of AKT/ERK-Dependent PDGF/HIF-1α In Vitro and In Vivo

التفاصيل البيبلوغرافية
العنوان: Caffeic Acid Phenethyl Ester Rescues Pulmonary Arterial Hypertension through the Inhibition of AKT/ERK-Dependent PDGF/HIF-1α In Vitro and In Vivo
المؤلفون: Chin-Chang Cheng, Pei-Ling Chi, Min-Ci Shen, Chih-Wen Shu, Shue-Ren Wann, Chun-Peng Liu, Ching-Jiunn Tseng, Wei-Chun Huang
المصدر: International Journal of Molecular Sciences, Vol 20, Iss 6, p 1468 (2019)
بيانات النشر: MDPI AG, 2019.
سنة النشر: 2019
المجموعة: LCC:Biology (General)
LCC:Chemistry
مصطلحات موضوعية: Caffeic acid phenethyl ester, hypoxia-inducible factor-1α, pulmonary arterial hypertension, pulmonary smooth muscle cell, apoptosis resistance, Biology (General), QH301-705.5, Chemistry, QD1-999
الوصف: Pulmonary arterial hypertension (PAH) is characterized by pulmonary arterial proliferation and remodeling, resulting in a specific increase in right ventricle systolic pressure (RVSP) and, ultimately right ventricular failure. Recent studies have demonstrated that caffeic acid phenethyl ester (CAPE) exerts a protective role in NF-κB-mediated inflammatory diseases. However, the effect of CAPE on PAH remains to be elucidated. In this study, monocrotaline (MCT) was used to establish PAH in rats. Two weeks after the induction of PAH by MCT, CAPE was administrated by intraperitoneal injection once a day for two weeks. Pulmonary hemodynamic measurements and pulmonary artery morphological assessments were examined. Our results showed that administration of CAPE significantly suppressed MCT-induced vascular remodeling by decreasing the HIF-1α expression and PDGF-BB production, and improved in vivo RV systolic performance in rats. Furthermore, CAPE inhibits hypoxia- and PDGF-BB-induced HIF-1α expression by decreasing the activation of the AKT/ERK pathway, which results in the inhibition of human pulmonary artery smooth muscle cells (hPASMCs) proliferation and prevention of cells resistant to apoptosis. Overall, our data suggest that HIF-1α is regarded as an alternative target for CAPE in addition to NF-κB, and may represent a promising therapeutic agent for the treatment of PAH diseases.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 1422-0067
Relation: https://www.mdpi.com/1422-0067/20/6/1468; https://doaj.org/toc/1422-0067
DOI: 10.3390/ijms20061468
URL الوصول: https://doaj.org/article/719603f5b38e41cd82524eb36e44984a
رقم الأكسشن: edsdoj.719603f5b38e41cd82524eb36e44984a
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:14220067
DOI:10.3390/ijms20061468