title: Effect of all-trans retinoic acids (ATRA) on the expression of α-smooth muscle actin (α-SMA) in the lung tissues of rats with pulmonary arterial hypertension (PAH).
abstract: The effect of all-trans retinoic acid (ATRA) on the expression of α-smooth muscle actin (α-SMA) in rats with pulmonary arterial hypertension (PAH) was studied, and the mechanism of the effect of ATRA on PAH was proposed. Thirty male SD rats were randomly divided into normal control, monocrotaline (MCT) model, and ATRA [30 mg/(kg.day)]intervention groups (N = 10 each). The mean pulmonary arterial pressure was recorded. Right ventricular hypertrophy index (RVHI) was calculated (weight of right ventricle: total weight of left ventricle and interventricular septum). The percentages of wall thickness of pulmonary arteriole (WT) to external diameter of artery (WT%) and vascular wall area (WA) to total vascular area (WA%) were determined. Real-time fluorescence-based quantitative PCR and western blot analyses were employed to detect the α-SMA mRNA and protein expressions. The mean pulmonary arterial pressure, RVHI, WT%, and WA% were all obviously higher in the model group than in the control and intervention groups. The values of these indicators in the intervention group were also higher than those in the control group (P < 0.01). The mRNA and protein expression levels of α-SMA were significantly higher in the lung tissue of model rats than those in the control and intervention groups. However, the intervention group showed no statistically significant differences in α-SMA mRNA and protein expression levels compared to the control (P < 0.05). ATRA inhibited the α-SMA mRNA and protein expressionin the lung tissues of rats with MCT-induced PAH, and could be used to treat PAH.
authors.affiliation: Department of Pediatrics, Affiliated Hospital of Jiangsu University, Zhenjiang, China.
authors.forename: Y
authors.initials: Y
authors.lastname: Xin
authors.affiliation: Department of Pediatrics, Affiliated Hospital of Jiangsu University, Zhenjiang, China.
authors.forename: J-Q
authors.initials: JQ
authors.lastname: Lv
authors.affiliation: Department of Pathology, Medical School of Jiangsu University, Zhenjiang, China.
authors.forename: Y-Z
authors.initials: YZ
authors.lastname: Wang
authors.affiliation: Department of Pediatrics, Affiliated Hospital of Jiangsu University, Zhenjiang, China.
authors.forename: J
authors.initials: J
authors.lastname: Zhang
authors.affiliation: Department of Pediatrics, Affiliated Hospital of Jiangsu University, Zhenjiang, China.
authors.forename: X
authors.initials: X
authors.lastname: Zhang
mesh_terms: D000199:Actins / Q000096:biosynthesis* / Q000235:genetics; D000818:Animals; D004195:Disease Models, Animal; D006976:Hypertension, Pulmonary / Q000139:chemically induced / Q000188:drug therapy* / Q000235:genetics / Q000378:metabolism*; D008168:Lung / Q000187:drug effects / Q000378:metabolism; D008297:Male; D016686:Monocrotaline; D011651:Pulmonary Artery / Q000187:drug effects; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D014212:Tretinoin / Q000494:pharmacology*
chemical_list: D000199:Actins; D016686:Monocrotaline; D012333:RNA, Messenger; D014212:Tretinoin; C498862:Acta2 protein, rat