Inhibition of mTORC1 renders cardiac protection against lipopolysaccharide

International Journal of Clinical and Experimental Pathology

Volumn 7, Issue 12, 2014, Pages 8432-8442

  Li, Xiang ^a,b   Jiang, Lijing ^a   Lin, Shenghui ^c   He, Yunfen ^d   Shen, Guofeng ^a   Cai, Zhenlin ^a   Ling, Meirong ^a   Ni, Jindi ^a   Zhang, Hao ^a   Zhang, Min ^b  

^a FUDAN UNIVERSITY   (China)

^b GANSU PROVINCIAL HOSPITAL   (China)

^c Department of Neurosurgery Jinjiang Hospital of Quanzhou Medical College   (China)

^d Minhang District Maternal and Child Health Hospital of Shanghai   (China)

Author keywords

Cardiac dysfunction; LPS; mTORC1; Rapamycin

Indexed keywords

IMMUNOSUPPRESSIVE AGENT; LIPOPOLYSACCHARIDE; MECHANISTIC TARGET OF RAPAMYCIN COMPLEX 1; MULTIPROTEIN COMPLEX; PROTEIN KINASE B; RAPAMYCIN; TARGET OF RAPAMYCIN KINASE;

ANIMAL; ANTAGONISTS AND INHIBITORS; APOPTOSIS; C57BL MOUSE; CELL LINE; CHEMICALLY INDUCED; COMPLICATION; DISEASE MODEL; DRUG EFFECTS; ECHOCARDIOGRAPHY; HEART; METABOLISM; MOUSE; PATHOPHYSIOLOGY; RAT; REAL TIME POLYMERASE CHAIN REACTION; SEPSIS; TUNEL ASSAY; WESTERN BLOTTING;

ANIMALS; APOPTOSIS; BLOTTING, WESTERN; CELL LINE; DISEASE MODELS, ANIMAL; ECHOCARDIOGRAPHY; HEART; IMMUNOSUPPRESSIVE AGENTS; IN SITU NICK-END LABELING; LIPOPOLYSACCHARIDES; MICE; MICE, INBRED C57BL; MULTIPROTEIN COMPLEXES; PROTO-ONCOGENE PROTEINS C-AKT; RATS; REAL-TIME POLYMERASE CHAIN REACTION; SEPSIS; SIROLIMUS; TOR SERINE-THREONINE KINASES;

EID: 84921448137     PISSN: None     EISSN: 19362625     Source Type: Journal    
DOI: None     Document Type: Article

References (22)

1. Flierl MA, Rittirsch D, Huber-Lang MS, Sarma JV and Ward PA. Molecular events in the cardiomyopathy of sepsis. Mol Med 2008; 14: 327-336.
2. Maeder M, Fehr T, Rickli H and Ammann P. Sepsis-associated myocardial dysfunction: diagnostic and prognostic impact of cardiac troponins and natriuretic peptides. Chest 2006; 129: 1349-1366.
3. Paoli G, Valente S, Ardissino D and Gensini GF. Myocardial dysfunction during sepsis: epidemiology, prognosis and treatment. G Ital Cardiol (Rome) 2011; 12: 804-814.
4. Balija TM and Lowry SF. Lipopolysaccharide and sepsis-associated myocardial dysfunction. Curr Opin Infect Dis 2011; 24: 248-253.
5. Kimball SR, Orellana RA, O'Connor PM, Suryawan A, Bush JA, Nguyen HV, Thivierge MC, Jefferson LS and Davis TA. Endotoxin induces differential regulation of mTOR-dependent sig-naling in skeletal muscle and liver of neonatal pigs. Am J Physiol Endocrinol Metab 2003; 285: E637-644.
6. Schaeffer V, Arbabi S, Garcia IA, Knoll ML, Cuschieri J, Bulger EM and Maier RV. Role of the mTOR pathway in LPS-activated monocytes: influence of hypertonic saline. J Surg Res 2011; 171: 769-776.
7. Chong ZZ, Shang YC and Maiese K. Cardiovascular disease and mTOR signaling. Trends Cardiovasc Med 2011; 21: 151-155.
8. Yang SS, Liu YB, Yu JB, Fan Y, Tang SY, Duan WT, Wang Z, Gan RT and Yu B. Rapamycin protects heart from ischemia/reperfusion injury independent of autophagy by activating PI3 kinase-Akt pathway and mitochondria K(ATP) channel. Pharmazie 2010; 65: 760-765.
9. Das A, Salloum FN, Durrant D, Ockaili R and Kukreja RC. Rapamycin protects against myocardial ischemia-reperfusion injury through JAK2-STAT3 signaling pathway. J Mol Cell Cardiol 2012; 53: 858-869.
10. Di R, Wu X, Chang Z, Zhao X, Feng Q, Lu S, Luan Q, Hemmings BA, Li X and Yang Z. S6K inhibition renders cardiac protection against myocardial infarction through PDK1 phosphorylation of Akt. Biochem J 2012; 441: 199-207.
11. Saunders RN, Metcalfe MS and Nicholson ML. Rapamycin in transplantation: a review of the evidence. Kidney Int 2001; 59: 3-16.
12. Wang Y, Yu X, Wang F, Li H, Lv X, Lu D and Wang H. Yohimbine promotes cardiac NE release and prevents LPS-induced cardiac dysfunction via blockade of presynaptic alpha2A-adrenergic receptor. PLoS One 2013; 8: e63622.
13. Respress JL and Wehrens XH. Transthoracic echocardiography in mice. J Vis Exp 2010.
14. Tien YC, Lin JY, Lai CH, Kuo CH, Lin WY, Tsai CH, Tsai FJ, Cheng YC, Peng WH and Huang CY. Carthamus tinctorius L. prevents LPS-induced TNF-alpha signaling activation and cell apoptosis through JNK1/2-NFkappaB pathway inhibition in H9c2 cardiomyoblast cells. J Ethnopharmacol 2010; 130: 505-513.
15. Hong F, Kwon SJ, Jhun BS, Kim SS, Ha J, Kim SJ, Sohn NW, Kang C and Kang I. Insulin-like growth factor-1 protects H9c2 cardiac myoblasts from oxidative stress-induced apoptosis via phosphatidylinositol 3-kinase and extracellular signal-regulated kinase pathways. Life Sci 2001; 68: 1095-1105.
16. Landesberg G, Gilon D, Meroz Y, Georgieva M, Levin PD, Goodman S, Avidan A, Beeri R, Weissman C, Jaffe AS and Sprung CL. Diastolic dysfunction and mortality in severe sepsis and septic shock. Eur Heart J 2012; 33: 895-903.
17. Flynn A, Chokkalingam Mani B and Mather PJ. Sepsis-induced cardiomyopathy: a review of pathophysiologic mechanisms. Heart Fail Rev 2010; 15: 605-611.
18. Yu X, Jia B, Wang F, Lv X, Peng X, Wang Y, Li H, Lu D and Wang H. Alpha (1) adrenoceptor activation by norepinephrine inhibits LPS-induced cardiomyocyte TNF-alpha production via modulating ERK1/2 and NF-kappaB pathway. J Cell Mol Med 2014; 18: 263-273.
19. Bishu K, Ogut O, Kushwaha S, Mohammed SF, Ohtani T, Xu X, Brozovich FV and Redfield MM. Anti-remodeling effects of rapamycin in experimental heart failure: dose response and interaction with Angiotensin receptor blockade. PLoS One 2013; 8: e81325.
20. Lassaletta AD, Elmadhun NY, Zanetti AV, Feng J, Anduaga J, Gohh RY, Sellke FW and Bianchi C. Rapamycin treatment of healthy pigs subjected to acute myocardial ischemia-reperfusion injury attenuates cardiac functions and increases myocardial necrosis. Ann Thorac Surg 2014; 97: 901-907.
21. Flynn JM, O'Leary MN, Zambataro CA, Academia EC, Presley MP, Garrett BJ, Zykovich A, Mooney SD, Strong R, Rosen CJ, Kapahi P, Nelson MD, Kennedy BK and Melov S. Late-life rapamycin treatment reverses age-related heart dysfunction. Aging Cell 2013; 12: 851-862.
22. Frost RA and Lang CH. mTor signaling in skeletal muscle during sepsis and inflammation: where does it all go wrong? Physiology (Bethesda) 2011; 26: 83-96.