Abstract
BackgroundEvidences suggest that β3 -adrenoceptor (β3-AR) plays an important role in heart failure (HF), although no data is reported indicating how these effects may change with the increasing age. Pulmonary congestion and edema are the major life-threatening complications associated with HF. The purpose of this study is to explore the relationship between the anti-β3-AR autoantibody and the expression of β3-AR in the lungs and heart for both aged patients and rats with HF.MethodsSynthetic β3-AR peptides served as the target antigens in ELISA were used to screen the anti-β3-AR autoantibody in aged patients and rats. Two aged rat models were constructed based on aortic banding and sham-operation. The expression of β3-AR mRNA and protein in the lung and heart was measured in intervention and non-intervention groups by Western blot analysis at the baseline, 5th, 7th, 9th and 11th week, respectively.ResultsThe frequency and titer of anti-β3-AR autoantibody in aged patients and rats with HF were higher than those in the control group (p<0.05). The expression of β3-AR mRNA and protein in pulmonary tissues decreased continually from the 7th week (p<0.05), followed by HF observed during the 9th week. The expression of β3-AR in myocardial tissues continued to increase after the 9th week (p<0.05), and the expression of both β3-AR mRNA and protein in the BRL group [HF group with BRL37344 (4-[-[2-hydroxy-(3-chlorophenyl)ethyl-amino] phenoxyacetic acid) (a β3-AR agonist) injection] was positively correlated with BRL37344 when compared with non-BRL group (HF group without BRL37344 injection) (p<0.05).ConclusionAnti-β3-AR autoantibody was detected in aged patients and rats with HF. The expression of β3-AR mRNA and protein in pulmonary tissues decreased continually, and began earlier than in the heart, but its expression in myocardial tissues increased continually and could be further promoted by β3-AR agonist.
Highlights
Growing evidences suggest that the autoimmune mechanism may play a major role in heart failure observed in both rats and human patients [1,2,3,4]
Previous studies have shown that autoantibodies against b-adrenoceptors display antagonist activity on the corresponding receptor and influence cardiac function [3,5,6] It has been well established that b-adrenoceptor (b-AR) belongs to the family of G-protein coupled receptors, and 3 subtypes (b1, b2 and b3-AR) have been associated with different changes in heart failure
The accumulative mortality rate in the BRL group was significantly higher than that in the non-BRL group (p,0.05, 32% vs. 12%), and these results suggested that b3AR agonist (BRL37344) might be associated with an increased risk of death in aged rats with heart failure
Summary
Growing evidences suggest that the autoimmune mechanism may play a major role in heart failure observed in both rats and human patients [1,2,3,4]. Some disagreement exists regarding the conclusions reported by these studies [8,12], indicating that the relationship between b3-AR and cardiac function warrants further investigation, in aged patients or rats with heart failure. Evidences suggest that b3-adrenoceptor (b3-AR) plays an important role in heart failure (HF), no data is reported indicating how these effects may change with the increasing age. The purpose of this study is to explore the relationship between the anti-b3-AR autoantibody and the expression of b3-AR in the lungs and heart for both aged patients and rats with HF
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