Decreased autophagy in rat heart induced by anti-β1-adrenergic receptor autoantibodies contributes to the decline in mitochondrial membrane potential.

It has been recognized that changes in mitochondrial structure plays a key role in development of cardiac dysfunction, and autophagy has been shown to exert maintenance of mitochondrial homeostasis effects. Our previous study found that anti-β1-adrenergic receptor autoantibodies (β1-AABs) could lead...

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Autores principales:	Li Wang, Keyi Lu, Haihu Hao, Xiaoyu Li, Jie Wang, Ke Wang, Jin Wang, Zi Yan, Suli Zhang, Yunhui Du, Huirong Liu
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2013
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/adcb081ef36f42f4a9b1f56ee80f062d
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spelling	oai:doaj.org-article:adcb081ef36f42f4a9b1f56ee80f062d2021-11-18T08:45:22ZDecreased autophagy in rat heart induced by anti-β1-adrenergic receptor autoantibodies contributes to the decline in mitochondrial membrane potential.1932-620310.1371/journal.pone.0081296https://doaj.org/article/adcb081ef36f42f4a9b1f56ee80f062d2013-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/24278413/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203It has been recognized that changes in mitochondrial structure plays a key role in development of cardiac dysfunction, and autophagy has been shown to exert maintenance of mitochondrial homeostasis effects. Our previous study found that anti-β1-adrenergic receptor autoantibodies (β1-AABs) could lead to cardiac dysfunction along with abnormalities in mitochondrial structure. The present study tested the hypothesis that β1-AABs may induce the decline in mitochondrial membrane potential (ΔΨm) by suppression of cardiac autophagy, which contributed to cardiac dysfunction. Male adult rats were randomized to receive a vehicle or peptide corresponding to the second extracellular loop of the β1 adrenergic receptor (β1-AAB group, 0.4 μg/g every two weeks for 12 weeks) and treated with rapamycin (RAPA, an autophagy agonist) at 5 mg/kg/day for two days before detection. At the 4th week, 8th week and 12th week of active immunization, the rats were sacrificed and cardiac function and the levels of cardiac LC3 and Beclin-1 were detected. ΔΨm in cardiac myocytes was determined by myocardial radionuclide imaging technology and JC-1 staining. In the present study, β1-AABs caused cardiac dysfunction, reduced ΔΨm and decreased cardiac autophagy. Treatment with RAPA markedly attenuated β1-AABs-induced cardiac injury evidenced by recovered ΔΨm. Taken together, these results suggested that β1-AABs exerted significant decreased ΔΨm, which may contribute to cardiac dysfunction, most likely by decreasing cardiac autophagy in vivo. Moreover, myocardial radionuclide imaging technology may be needed to assess the risk in developing cardiac dysfunction for the people who have β1-AABs in their blood.Li WangKeyi LuHaihu HaoXiaoyu LiJie WangKe WangJin WangZi YanSuli ZhangYunhui DuHuirong LiuPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 8, Iss 11, p e81296 (2013)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Li Wang Keyi Lu Haihu Hao Xiaoyu Li Jie Wang Ke Wang Jin Wang Zi Yan Suli Zhang Yunhui Du Huirong Liu Decreased autophagy in rat heart induced by anti-β1-adrenergic receptor autoantibodies contributes to the decline in mitochondrial membrane potential.
description	It has been recognized that changes in mitochondrial structure plays a key role in development of cardiac dysfunction, and autophagy has been shown to exert maintenance of mitochondrial homeostasis effects. Our previous study found that anti-β1-adrenergic receptor autoantibodies (β1-AABs) could lead to cardiac dysfunction along with abnormalities in mitochondrial structure. The present study tested the hypothesis that β1-AABs may induce the decline in mitochondrial membrane potential (ΔΨm) by suppression of cardiac autophagy, which contributed to cardiac dysfunction. Male adult rats were randomized to receive a vehicle or peptide corresponding to the second extracellular loop of the β1 adrenergic receptor (β1-AAB group, 0.4 μg/g every two weeks for 12 weeks) and treated with rapamycin (RAPA, an autophagy agonist) at 5 mg/kg/day for two days before detection. At the 4th week, 8th week and 12th week of active immunization, the rats were sacrificed and cardiac function and the levels of cardiac LC3 and Beclin-1 were detected. ΔΨm in cardiac myocytes was determined by myocardial radionuclide imaging technology and JC-1 staining. In the present study, β1-AABs caused cardiac dysfunction, reduced ΔΨm and decreased cardiac autophagy. Treatment with RAPA markedly attenuated β1-AABs-induced cardiac injury evidenced by recovered ΔΨm. Taken together, these results suggested that β1-AABs exerted significant decreased ΔΨm, which may contribute to cardiac dysfunction, most likely by decreasing cardiac autophagy in vivo. Moreover, myocardial radionuclide imaging technology may be needed to assess the risk in developing cardiac dysfunction for the people who have β1-AABs in their blood.
format	article
author	Li Wang Keyi Lu Haihu Hao Xiaoyu Li Jie Wang Ke Wang Jin Wang Zi Yan Suli Zhang Yunhui Du Huirong Liu
author_facet	Li Wang Keyi Lu Haihu Hao Xiaoyu Li Jie Wang Ke Wang Jin Wang Zi Yan Suli Zhang Yunhui Du Huirong Liu
author_sort	Li Wang
title	Decreased autophagy in rat heart induced by anti-β1-adrenergic receptor autoantibodies contributes to the decline in mitochondrial membrane potential.
title_short	Decreased autophagy in rat heart induced by anti-β1-adrenergic receptor autoantibodies contributes to the decline in mitochondrial membrane potential.
title_full	Decreased autophagy in rat heart induced by anti-β1-adrenergic receptor autoantibodies contributes to the decline in mitochondrial membrane potential.
title_fullStr	Decreased autophagy in rat heart induced by anti-β1-adrenergic receptor autoantibodies contributes to the decline in mitochondrial membrane potential.
title_full_unstemmed	Decreased autophagy in rat heart induced by anti-β1-adrenergic receptor autoantibodies contributes to the decline in mitochondrial membrane potential.
title_sort	decreased autophagy in rat heart induced by anti-β1-adrenergic receptor autoantibodies contributes to the decline in mitochondrial membrane potential.
publisher	Public Library of Science (PLoS)
publishDate	2013
url	https://doaj.org/article/adcb081ef36f42f4a9b1f56ee80f062d
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Decreased autophagy in rat heart induced by anti-β1-adrenergic receptor autoantibodies contributes to the decline in mitochondrial membrane potential.

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