Hypercholesterolemia downregulates autophagy in the rat heart

Background: We have previously shown that efficiency of ischemic conditioning is diminished in hypercholesterolemia and that autophagy is necessary for cardioprotection. However, it is unknown whether isolated hypercholesterolemia disturbs autophagy or the mammalian target of rapamycin (mTOR) pathwa...

Teljes leírás

Elmentve itt :
Bibliográfiai részletek
Szerzők: Giricz Zoltán
Koncsos Gábor
Rajtík Tomáš
Varga Zoltán
Baranyai Tamás
Csonka Csaba
Szobi Adrián
Adameová Adriana
Gottlieb Roberta A.
Ferdinandy Péter
Dokumentumtípus: Cikk
Megjelent: 2017
Sorozat:LIPIDS IN HEALTH AND DISEASE 16 No. 1
Tárgyszavak:
doi:10.1186/s12944-017-0455-0

mtmt:3192151
Online Access:http://publicatio.bibl.u-szeged.hu/27947
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490 0 |a LIPIDS IN HEALTH AND DISEASE  |v 16 No. 1 
520 3 |a Background: We have previously shown that efficiency of ischemic conditioning is diminished in hypercholesterolemia and that autophagy is necessary for cardioprotection. However, it is unknown whether isolated hypercholesterolemia disturbs autophagy or the mammalian target of rapamycin (mTOR) pathways. Therefore, we investigated whether isolated hypercholesterolemia modulates cardiac autophagy-related pathways or programmed cell death mechanisms such as apoptosis and necroptosis in rat heart. Methods: Male Wistar rats were fed either normal chow (NORM; n=9) or with 2% cholesterol and 0.25% cholic acid-enriched diet (CHOL; n=9) for 12 weeks. CHOL rats exhibited a 41% increase in plasma total cholesterol level over that of NORM rats (4.09mmol/L vs. 2.89mmol/L) at the end of diet period. Animals were sacrificed, hearts were excised and briefly washed out. Left ventricles were snap-frozen for determination of markers of autophagy, mTOR pathway, apoptosis, and necroptosis by Western blot. Results: Isolated hypercholesterolemia was associated with a significant reduction in expression of cardiac autophagy markers such as LC3-II, Beclin-1, Rubicon and RAB7 as compared to controls. Phosphorylation of ribosomal S6, a surrogate marker for mTOR activity, was increased in CHOL samples. Cleaved caspase-3, a marker of apoptosis, increased in CHOL hearts, while no difference in the expression of necroptotic marker RIP1, RIP3 and MLKL was detected between treatments. Conclusions: This is the first comprehensive analysis of autophagy and programmed cell death pathways of apoptosis and necroptosis in hearts of hypercholesterolemic rats. Our data show that isolated hypercholesterolemia suppresses basal cardiac autophagy and that the decrease in autophagy may be a result of an activated mTOR pathway. Reduced autophagy was accompanied by increased apoptosis, while cardiac necroptosis was not modulated by isolated hypercholesterolemia. Decreased basal autophagy and elevated apoptosis may be responsible for the loss of cardioprotection reported in hypercholesterolemic animals. 
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700 0 1 |a Koncsos Gábor  |e aut 
700 0 1 |a Rajtík Tomáš  |e aut 
700 0 1 |a Varga Zoltán  |e aut 
700 0 1 |a Baranyai Tamás  |e aut 
700 0 1 |a Csonka Csaba  |e aut 
700 0 1 |a Szobi Adrián  |e aut 
700 0 1 |a Adameová Adriana  |e aut 
700 0 1 |a Gottlieb Roberta A.  |e aut 
700 0 1 |a Ferdinandy Péter  |e aut 
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