247
Views
5
CrossRef citations to date
0
Altmetric
Original Articles

Left ventricular hypertrophy is associated with overexpression of HSP60, TLR2, and TLR4 in the myocardium

, , , ORCID Icon, & ORCID Icon
Pages 236-246 | Received 27 Aug 2019, Accepted 02 Feb 2020, Published online: 14 Feb 2020

References

  • Catalucci D, Latronico MVG, Ellingsen O, et al. Physiological myocardial hypertrophy: how and why? Front Biosci. 2008;13(13):312–324.
  • Stanton T, Dunn FG. Hypertension, left ventricular hypertrophy, and myocardial ischemia. Med Clin North Am. 2017;101(1):29–41.
  • Tham YK, Bernardo BC, Ooi JYY, et al. Pathophysiology of cardiac hypertrophy and heart failure: signaling pathways and novel therapeutic targets. Arch Toxicol. 2015;89(9):1401–1438.
  • Tseng ZH, Olgin JE, Vittinghoff E, et al. Prospective countywide surveillance and autopsy characterization of sudden cardiac death: POST SCD study. Circulation. 2018;137(25):2689–2700.
  • Rosca MG, Tandler B, Hoppel CL. Mitochondria in cardiac hypertrophy and heart failure. J Mol Cell Cardiol. 2013;55:31–41.
  • Zhang J. Myocardial energetics in cardiac hypertrophy. Clin Exp Pharmacol Physiol. 2002;29(4):351–359.
  • Meng Q, Li BX, Xiao X. Toward developing chemical modulators of hsp60 as potential therapeutics. Front Mol Biosci. 2018;5:35.
  • Lin KM, Lin B, Lian IY, et al. Combined and individual mitochondrial HSP60 and HSP10 expression in cardiac myocytes protects mitochondrial function and prevents apoptotic cell deaths induced by simulated ischemia-reoxygenation. Circulation. 2001;103(13):1787–1792.
  • Kirchhoff SR, Gupta S, Knowlton AA. Cytosolic heat shock protein 60, apoptosis, and myocardial injury. Circulation. 2002;105(24):2899–2904.
  • Gupta S, Knowlton AA. Cytosolic heat shock protein 60, hypoxia, and apoptosis. Circulation. 2002;106(21):2727–2733.
  • Knowlton A, Gupta S. HSP60, Bax, and cardiac apoptosis. Cardiovasc Toxicol. 2003;3(3):263–268.
  • Gupta S, Knowlton AA. HSP60 trafficking in adult cardiac myocytes: role of the exosomal pathway. Am J Physiol Heart Circ Physiol. 2007;292(6):H3052–6.
  • Graham PA, Ruhia W, Carola L, et al. Circulating heat shock protein 60 is associated with early cardiovascular disease. Hypertension. 2000;36:303–307.
  • Ohashi K, Burkart V, Flohe S, et al. Cutting edge: heat shock protein 60 is a putative endogenous ligand of the toll-like receptor-4 complex. J Immunol. 2000;164(2):558–561.
  • Mitchell JA, Ryffel B, Quesniaux VFJ, et al. Role of pattern-recognition receptors in cardiovascular health and disease. Biochem Soc Trans. 2007;35(6):1449–1452.
  • Yang Y, Lv J, Jiang S, et al. The emerging role of Toll-like receptor 4 in myocardial inflammation. Cell Death Dis. 2016;7(5):e2234–e2234.
  • Yu L, Feng Z. The role of toll-like receptor signaling in the progression of heart failure. Mediators Inflamm. 2018;2018:1–11.
  • Tian J, Guo X, Liu X-M, et al. Extracellular HSP60 induces inflammation through activating and up-regulating TLRs in cardiomyocytes. Cardiovasc Res. 2013;98(3):391–401.
  • Li F, Zhang H, Yang L, et al. NLRP3 deficiency accelerates pressure overload-induced cardiac remodeling via increased TLR4 expression. J Mol Med. 2018;96(11):1189–1202.
  • Ehrentraut H, Felix Ehrentraut S, Boehm O, et al. Tlr4 deficiency protects against cardiac pressure overload induced hyperinflammation. PLOS One. 2015;10(11):e0142921.
  • Basso C, , Aguilera B, Banner J, et al. Guidelines for autopsy investigation of sudden cardiac death: 2017 update from the Association for European Cardiovascular Pathology. Virchows Arch. 2017;471(6):691–705.
  • Mrakovcic-Sutic I, Jakovac H, Simin M, et al. Heat shock protein-GP96 as an innate sensor of damage and activator of autoreactive NKT and regulatory T cells during liver regeneration. Histol Histopathol. 2008;23:1111–1126.
  • Jakovac H, Grubić Kezele T, Radošević-Stašić B. Expression profiles of metallothionein I/II and megalin in cuprizone model of de- and remyelination. Neuroscience. 2018;388:69–86.
  • Li Y, Si R, Feng Y, et al. Myocardial ischemia activates an injurious innate immune signaling via cardiac heat shock protein 60 and Toll-like receptor 4. J Biol Chem. 2011;286(36):31308–31319.
  • Wang Y, Chen L, Hagiwara N, et al. Regulation of heat shock protein 60 and 72 expression in the failing heart. J Mol Cell Cardiol. 2010;48(2):360–366.
  • Liu L, Wang Y, Cao Z-Y, et al. Up-regulated TLR4 in cardiomyocytes exacerbates heart failure after long-term myocardial infarction. J Cell Mol Med. 2015;19(12):2728–2740.
  • Panneerselvam L, Raghunath A, Perumal E. Differential expression of myocardial heat shock proteins in rats acutely exposed to fluoride. Cell Stress Chaperones. 2017;22(5):743–750.
  • Knowlton AA. Paying for the tolls: the high cost of the innate immune system for the cardiac myocyte. Adv Exp Med Biol. 2017;1003:17–34.
  • Malik ZA, Kott KS, Poe AJ, et al. Cardiac myocyte exosomes: stability, HSP60, and proteomics. Am J Physiol Heart Circ Physiol. 2013;304(7):H954–65.
  • Bonanad C, Nunez J, Sanchis J, et al. Serum heat shock protein 60 in acute heart failure: a new biomarker?. Congest Heart Fail. 2013;19(1):6–10.
  • Matsuda S, Umemoto S, Yoshimura K, et al. Angiotensin activates MCP-1 and induces cardiac hypertrophy and dysfunction via toll-like receptor 4. J Atheroscler Thromb. 2015;22(8):833–844.
  • Katare PB, Bagul PK, Dinda AK, et al. Toll-like receptor 4 inhibition improves oxidative stress and mitochondrial health in isoproterenol-induced cardiac hypertrophy in rats. Front Immunol. 2017;8:719.
  • Monnerat-Cahli G, Alonso H, Gallego M, et al. Toll-like receptor 4 activation promotes cardiac arrhythmias by decreasing the transient outward potassium current (Ito) through an IRF3-dependent and MyD88-independent pathway. J Mol Cell Cardiol. 2014;76:116–125.
  • Chen T-H, Liu S-W, Chen M-R, et al. Neonatal death and heart failure in mouse with transgenic HSP60 expression. Biomed Res Int. 2015;2015:539805.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.