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Cardiac apoptosis caused by elevated cholesterol level in experimental autoimmune myocarditis.

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.

journal_name

Exp Cell Res

journal_title

Experimental cell research

authors

Chang H,Wang Y,Wu Y,Ma P,Song Y,Liu C,Ye Y,Qi JH,Qi Z

doi

10.1016/j.yexcr.2020.112169

subject

Has Abstract

pub_date

2020-10-01 00:00:00

pages

112169

issue

1

eissn

0014-4827

issn

1090-2422

pii

S0014-4827(20)30418-3

journal_volume

395

pub_type

杂志文章

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