Abstract
Pulmonary arterial hypertension (PAH) is a progressive disease which causes right ventricular (RV) failure. Canstatin, a C-terminal fragment of type IV collagen α2 chain, is expressed in various rat organs. However, the expression level of canstatin in plasma and organs during PAH is still unclear. We aimed to clarify it and further investigated the protective effects of canstatin in a rat model of monocrotaline-induced PAH. Cardiac functions were assessed by echocardiography. Expression levels of canstatin in plasma and organs were evaluated by enzyme-linked immunosorbent assay and Western blotting, respectively. PAH was evaluated by catheterization. RV remodeling was evaluated by histological analyses. Real-time polymerase chain reaction was performed to evaluate RV remodeling-related genes. The plasma concentration of canstatin in PAH rats was decreased, which was correlated with a reduction in acceleration time/ejection time ratio and an increase in RV weight/body weight ratio. The protein expression of canstatin in RV, lung and kidney was decreased in PAH rats. While recombinant canstatin had no effect on PAH, it significantly improved RV remodeling, including hypertrophy and fibrosis, and prevented the increase in RV remodeling-related genes. We demonstrated that plasma canstatin is decreased in PAH rats and that administration of canstatin exerts cardioprotective effects.
Highlights
Pulmonary arterial hypertension (PAH) is a progressive disease characterized by an abnormal elevation of mean PA pressure with PA remodeling [1]
Plasma Concentration of Canstatin Was Decreased in PAH Rats, Which Was Correlated with Pathological Conditions
We evaluated the correlation between plasma concentration of canstatin and pathological conditions of PAH rats
Summary
Pulmonary arterial hypertension (PAH) is a progressive disease characterized by an abnormal elevation of mean PA pressure with PA remodeling [1]. To the best of our knowledge, the expression level of canstatin in human organs is currently unknown. We previously demonstrated that canstatin is highly expressed in rat organs including heart and lung [6]. We previously demonstrated that expression of canstatin was decreased in the infarcted area of myocardial infarction model rats [6,7]. The expression level of canstatin may be changed by different cardiovascular diseases. It is not clear whether the expression level is altered in PAH
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