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Cardiac apoptosis caused by elevated cholesterol level in experimental autoimmune myocarditis.
Exp Cell Res. 2020 Jul 09 [Online ahead of print]EC

Abstract

It has been reported that cholesterol-lowing agents can ameliorate severity of myocarditis. However, the beneficial effect of the agents has been claimed to be independent of cholesterol reduction as there is no significant change in the plasma cholesterol level in myocarditis. In the present study, using experimental autoimmune myocarditis (EAM) rats as an animal model, we demonstrated that EAM induced elevation of cholesterol level and impaired cholesterol efflux capacity in the cardiac tissue. Moreover, serum high-density lipoprotein (HDL) content was reduced and HDL function associated protein Paraoxonase 1 (PON1) activity was decreased. Besides, the major structural protein within HDL, Apolipoprotein A1 (ApoA1) expression in the cardiac tissues was significantly reduced while the level of serum ApoA1 was not significantly altered. Importantly, cholesterol depleting agent methyl-β-cyclodextrin (MβCD) alleviated the development of EAM, as monitored by decreased ratio of heart weight to body weight (HW/BW), decreased infiltration of inflammatory cells and collagen deposition, improved cardiac function, reduced expression of apoptosis-related protein Bax, Fas, FasL and caspase-3 and increased level of anti-apoptotic protein Bcl-2. These results suggest that reduction of cholesterol level in cardiac tissue could suppress EAM-induced cardiac apoptosis through both intrinsic and extrinsic apoptotic pathways.

Authors+Show Affiliations

School of Medicine, Xiamen University, Xiamen, 361102, China; Department of Geriatrics, Xiang'an Hospital of Xiamen University, Xiamen, 361100, China. Electronic address: changhe@xmu.edu.cn.School of Medicine, Xiamen University, Xiamen, 361102, China.School of Medicine, Xiamen University, Xiamen, 361102, China.School of Medicine, Xiamen University, Xiamen, 361102, China.School of Medicine, Xiamen University, Xiamen, 361102, China.School of Medicine, Xiamen University, Xiamen, 361102, China.College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, 310058, China.College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, 310058, China.School of Medicine, Xiamen University, Xiamen, 361102, China. Electronic address: qizhi@xmu.edu.cn.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

32653410

Citation

Chang, He, et al. "Cardiac Apoptosis Caused By Elevated Cholesterol Level in Experimental Autoimmune Myocarditis." Experimental Cell Research, 2020, p. 112169.
Chang H, Wang Y, Wu Y, et al. Cardiac apoptosis caused by elevated cholesterol level in experimental autoimmune myocarditis. Exp Cell Res. 2020.
Chang, H., Wang, Y., Wu, Y., Ma, P., Song, Y., Liu, C., Ye, Y., Qi, J. H., & Qi, Z. (2020). Cardiac apoptosis caused by elevated cholesterol level in experimental autoimmune myocarditis. Experimental Cell Research, 112169. https://doi.org/10.1016/j.yexcr.2020.112169
Chang H, et al. Cardiac Apoptosis Caused By Elevated Cholesterol Level in Experimental Autoimmune Myocarditis. Exp Cell Res. 2020 Jul 9;112169. PubMed PMID: 32653410.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Cardiac apoptosis caused by elevated cholesterol level in experimental autoimmune myocarditis. AU - Chang,He, AU - Wang,Yue, AU - Wu,Yang, AU - Ma,Ping, AU - Song,Ying, AU - Liu,Chunxiao, AU - Ye,Ying, AU - Qi,Jian-Hua, AU - Qi,Zhi, Y1 - 2020/07/09/ PY - 2020/03/04/received PY - 2020/07/02/revised PY - 2020/07/06/accepted PY - 2020/7/13/entrez PY - 2020/7/13/pubmed PY - 2020/7/13/medline KW - Cardiac apoptosis KW - Cholesterol KW - Experimental autoimmune myocarditis (EAM) KW - High-density lipoprotein (HDL) KW - Methyl-β-cyclodextrin (MβCD) SP - 112169 EP - 112169 JF - Experimental cell research JO - Exp. Cell Res. N2 - It has been reported that cholesterol-lowing agents can ameliorate severity of myocarditis. However, the beneficial effect of the agents has been claimed to be independent of cholesterol reduction as there is no significant change in the plasma cholesterol level in myocarditis. In the present study, using experimental autoimmune myocarditis (EAM) rats as an animal model, we demonstrated that EAM induced elevation of cholesterol level and impaired cholesterol efflux capacity in the cardiac tissue. Moreover, serum high-density lipoprotein (HDL) content was reduced and HDL function associated protein Paraoxonase 1 (PON1) activity was decreased. Besides, the major structural protein within HDL, Apolipoprotein A1 (ApoA1) expression in the cardiac tissues was significantly reduced while the level of serum ApoA1 was not significantly altered. Importantly, cholesterol depleting agent methyl-β-cyclodextrin (MβCD) alleviated the development of EAM, as monitored by decreased ratio of heart weight to body weight (HW/BW), decreased infiltration of inflammatory cells and collagen deposition, improved cardiac function, reduced expression of apoptosis-related protein Bax, Fas, FasL and caspase-3 and increased level of anti-apoptotic protein Bcl-2. These results suggest that reduction of cholesterol level in cardiac tissue could suppress EAM-induced cardiac apoptosis through both intrinsic and extrinsic apoptotic pathways. SN - 1090-2422 UR - https://www.unboundmedicine.com/medline/citation/32653410/Cardiac_apoptosis_caused_by_elevated_cholesterol_level_in_experimental_autoimmune_myocarditis L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014-4827(20)30418-3 DB - PRIME DP - Unbound Medicine ER -
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