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Gene expression of endothelin-1 and endothelin receptor a on monocrotaline-induced pulmonary hypertension in rats after bosentan treatment.

Lim KA, Kim KC, Cho MS, Lee BE, Kim HS, Hong YM - Korean Circ J (2010)

Bottom Line: Quantitative analysis of peripheral pulmonary arteries revealed that the increase in medial wall thickness after MCT injection was significantly attenuated in the bosentan group on day 28 and 42.In addition, the increase in the number of intra-acinar muscular arteries after MCT injection was reduced by bosentan on day 14, 28 and 42.The levels of ET-1 and ERA gene expression were significantly increased in the MCT group compared with control group on day 5, and bosentan decreased the expression of ET-1 on day 5.

View Article: PubMed Central - PubMed

Affiliation: Department of Pediatrics, College of Medicine, CHA University, Pocheon, Korea.

ABSTRACT

Background and objectives: Endothelin (ET)-1, a potent endothelium-derived vasoconstrictor peptide, has a potential pathophysiologic role in pulmonary hypertension. Bosentan, a dual ET receptor (ET(A)/ET(B)) antagonist, is efficacious in treatment of pulmonary hypertension. The objectives of this study were to investigate the expression of ET-1 and ET receptor A (ERA) genes and to evaluate the effect of bosentan in monocrotaline (MCT)-induced pulmonary hypertension.

Materials and methods: Four-week-old male Sprague-Dawley rats were treated as follows: control (n=36), subcutaneous (sc) injection of saline; MCT (n=36), sc injection of MCT (60 mg/kg); and bosentan (n=36), sc injection of MCT (60 mg/kg) plus 25 mg/kg/day bosentan orally.

Results: Serum ET-1 concentrations in the MCT group were higher than the control group on day 28 and 42. Quantitative analysis of peripheral pulmonary arteries revealed that the increase in medial wall thickness after MCT injection was significantly attenuated in the bosentan group on day 28 and 42. In addition, the increase in the number of intra-acinar muscular arteries after MCT injection was reduced by bosentan on day 14, 28 and 42. The levels of ET-1 and ERA gene expression were significantly increased in the MCT group compared with control group on day 5, and bosentan decreased the expression of ET-1 on day 5.

Conclusion: ET-1 contributes to the progression of cardiopulmonary pathology in rats with MCT-induced pulmonary hypertension. Administration of bosentan reduced ET-1 gene expression in MCT-induced pulmonary hypertension in rats.

No MeSH data available.


Related in: MedlinePlus

Hematoxylin-eosin staining of lung tissue. Monocrotaline (MCT) treatment thickened the muscular layer of the pulmonary arteriole at 42 days (B) compared to controls (A), and bosentan blocked this effect (C). Magnification: ×400.
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Figure 1: Hematoxylin-eosin staining of lung tissue. Monocrotaline (MCT) treatment thickened the muscular layer of the pulmonary arteriole at 42 days (B) compared to controls (A), and bosentan blocked this effect (C). Magnification: ×400.

Mentions: The basic pulmonary architecture was similar in each group. The predominant changes in pulmonary vasculature included the development of medial thickening in the pulmonary arterioles in the MCT group compared with control and bosentan group (Fig. 1). Quantitative analysis of the peripheral pulmonary arteries demonstrated that bosentan attenuated the increase wall thickness after MCT injection on day 28 and 42 (Fig. 2). Bosentan also attenuated the increased number of intra-acinar muscular arteries induced by MCT on day 1, 14, 28 (Fig. 3).


Gene expression of endothelin-1 and endothelin receptor a on monocrotaline-induced pulmonary hypertension in rats after bosentan treatment.

Lim KA, Kim KC, Cho MS, Lee BE, Kim HS, Hong YM - Korean Circ J (2010)

Hematoxylin-eosin staining of lung tissue. Monocrotaline (MCT) treatment thickened the muscular layer of the pulmonary arteriole at 42 days (B) compared to controls (A), and bosentan blocked this effect (C). Magnification: ×400.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2957645&req=5

Figure 1: Hematoxylin-eosin staining of lung tissue. Monocrotaline (MCT) treatment thickened the muscular layer of the pulmonary arteriole at 42 days (B) compared to controls (A), and bosentan blocked this effect (C). Magnification: ×400.
Mentions: The basic pulmonary architecture was similar in each group. The predominant changes in pulmonary vasculature included the development of medial thickening in the pulmonary arterioles in the MCT group compared with control and bosentan group (Fig. 1). Quantitative analysis of the peripheral pulmonary arteries demonstrated that bosentan attenuated the increase wall thickness after MCT injection on day 28 and 42 (Fig. 2). Bosentan also attenuated the increased number of intra-acinar muscular arteries induced by MCT on day 1, 14, 28 (Fig. 3).

Bottom Line: Quantitative analysis of peripheral pulmonary arteries revealed that the increase in medial wall thickness after MCT injection was significantly attenuated in the bosentan group on day 28 and 42.In addition, the increase in the number of intra-acinar muscular arteries after MCT injection was reduced by bosentan on day 14, 28 and 42.The levels of ET-1 and ERA gene expression were significantly increased in the MCT group compared with control group on day 5, and bosentan decreased the expression of ET-1 on day 5.

View Article: PubMed Central - PubMed

Affiliation: Department of Pediatrics, College of Medicine, CHA University, Pocheon, Korea.

ABSTRACT

Background and objectives: Endothelin (ET)-1, a potent endothelium-derived vasoconstrictor peptide, has a potential pathophysiologic role in pulmonary hypertension. Bosentan, a dual ET receptor (ET(A)/ET(B)) antagonist, is efficacious in treatment of pulmonary hypertension. The objectives of this study were to investigate the expression of ET-1 and ET receptor A (ERA) genes and to evaluate the effect of bosentan in monocrotaline (MCT)-induced pulmonary hypertension.

Materials and methods: Four-week-old male Sprague-Dawley rats were treated as follows: control (n=36), subcutaneous (sc) injection of saline; MCT (n=36), sc injection of MCT (60 mg/kg); and bosentan (n=36), sc injection of MCT (60 mg/kg) plus 25 mg/kg/day bosentan orally.

Results: Serum ET-1 concentrations in the MCT group were higher than the control group on day 28 and 42. Quantitative analysis of peripheral pulmonary arteries revealed that the increase in medial wall thickness after MCT injection was significantly attenuated in the bosentan group on day 28 and 42. In addition, the increase in the number of intra-acinar muscular arteries after MCT injection was reduced by bosentan on day 14, 28 and 42. The levels of ET-1 and ERA gene expression were significantly increased in the MCT group compared with control group on day 5, and bosentan decreased the expression of ET-1 on day 5.

Conclusion: ET-1 contributes to the progression of cardiopulmonary pathology in rats with MCT-induced pulmonary hypertension. Administration of bosentan reduced ET-1 gene expression in MCT-induced pulmonary hypertension in rats.

No MeSH data available.


Related in: MedlinePlus