2012Jiepou kexue jinzhanRequires access

Fluoxetine influences the expression of BMPR2 and prevents monocrotaline-induced pulmonary arterial hypertension in rats

Huailiang Wang

Open publisher page 0 citations

Abstract

Objective To investigate the influence of fluoxetine on bone morphogenetic protein receptor 2(BMPR2) expression in the pulmonary arteries and the preventive effect of fluoxetine on monocrotaline(MCT)-induced pulmonary arterial hypertension(PAH) in rats.Methods Twenty-four Wistar rats were randomly divided into 3 groups: control group,MCT group and fluoxetine-treated group.The hemodynamic measurements were recorded by Polygraph System.Morphological changes of the pulmonary arteries were observed by hematoxyline-eosine(HE).BMPR2 mRNA levels in the pulmonary arteries were detected by RT-PCR.Results Compared with the control group,MCT caused pulmonary arterial hypertension and the significant increases in the medial wall thickness percentage of the pulmonary arteries and right ventricle hypertrophic indexes,and reduced the expression of BMPR2 in the pulmonary arteries(0.01).After fluoxetine-treatment,the pulmonary arterial remodelling and the right ventricle hypertrophy were markedly inhibited and BMPR2 mRNA level was significantly reversed by fluoxetine(0.05).Conclusion Pulmonary arterial remodelling was probably associated with the reduction of BMPR2 expression in the pulmonary arteries,prevented PAH by fluoxetine might be related to reversing BMPR2 expression.

About this research paper

What this paper is about

Objective To investigate the influence of fluoxetine on bone morphogenetic protein receptor 2(BMPR2) expression in the pulmonary arteries and the preventive effect of fluoxetine on monocrotaline(MCT)-induced pulmonary arterial hypertension(PAH) in rats.Methods Twenty-four Wistar rats were randomly divided into 3 groups: control group,MCT group and fluoxetine-treated group.The hemodynamic measurements were recorded by Polygraph System.Morphological changes of the pulmonary arteries were observed by hematoxyline-eosine(HE).BMPR2 mRNA levels in the pulmonary arteries were detected by RT-PCR.Results Compared with the control group,MCT caused pulmonary arterial hypertension and the significant increases in the medial wall thickness percentage of the pulmonary arteries and right ventricle hypertrophic indexes,and reduced the expression of BMPR2 in the pulmonary arteries(0.01).After fluoxetine-treatment,the pulmonary arterial remodelling and the right ventricle hypertrophy were markedly inhibited and BMPR2 mRNA level was significantly reversed by fluoxetine(0.05).Conclusion Pulmonary arterial remodelling was probably associated with the reduction of BMPR2 expression in the pulmonary arteries,prevented PAH by fluoxetine might be related to reversing BMPR2 expression.

Why it matters

A significance statement is not available in the OpenAlex record.

Key contribution

A contribution statement is not available in the OpenAlex record.

Method / approach

Method details are not available in the OpenAlex metadata.

Main findings

Findings are not separately available in the OpenAlex metadata.

Limitations

Limitations are not available in the OpenAlex metadata.

Applications

Application details are not available in the OpenAlex metadata.

Available abstract

Objective To investigate the influence of fluoxetine on bone morphogenetic protein receptor 2(BMPR2) expression in the pulmonary arteries and the preventive effect of fluoxetine on monocrotaline(MCT)-induced pulmonary arterial hypertension(PAH) in rats.Methods Twenty-four Wistar rats were randomly divided into 3 groups: control group,MCT group and fluoxetine-treated group.The hemodynamic measurements were recorded by Polygraph System.Morphological changes of the pulmonary arteries were observed by hematoxyline-eosine(HE).BMPR2 mRNA levels in the pulmonary arteries were detected by RT-PCR.Results Compared with the control group,MCT caused pulmonary arterial hypertension and the significant increases in the medial wall thickness percentage of the pulmonary arteries and right ventricle hypertrophic indexes,and reduced the expression of BMPR2 in the pulmonary arteries(0.01).After fluoxetine-treatment,the pulmonary arterial remodelling and the right ventricle hypertrophy were markedly inhibited and BMPR2 mRNA level was significantly reversed by fluoxetine(0.05).Conclusion Pulmonary arterial remodelling was probably associated with the reduction of BMPR2 expression in the pulmonary arteries,prevented PAH by fluoxetine might be related to reversing BMPR2 expression.

Key concepts: BMPR2, Ventricle, Pulmonary hypertension, Fluoxetine, Internal medicine, Right ventricular hypertrophy, Pulmonary artery, Medicine

Related papers

Back to paper searchBrowse research topicsOriginal source
Fluoxetine influences the expression of BMPR2 and prevents monocrotaline-induced pulmonary arterial hypertension in rats — Research Paper | ScholarLens