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ISSN (Print): 1381-6128
ISSN (Online): 1873-4286

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Review Article

Heat Shock Protein 70 kDa as a Target for Diagnostics and Therapy of Cardiovascular and Cerebrovascular Diseases

Author(s): Ekaterina V. Konstantinova, Natalia S. Chipigina, Marina H. Shurdumova, E.I. Kovalenko and Alexander M. Sapozhnikov*

Volume 25, Issue 6, 2019

Page: [710 - 714] Pages: 5

DOI: 10.2174/1381612825666190329123924

Price: $65

Abstract

Acute focal ischemia is a main factor of pathogenesis of a number of widespread cardiovascular and cerebrovascular diseases, in particular, myocardial infarction and ischemic stroke. It is known that under the conditions of ischemia expression of intracellular heat shock proteins (HSPs), especially HSP70, grows greatly irrespective of the cell type. This stress-induced cell response is connected with cytoprotective properties of HSP70. The protective functions of HSP70 contribute to the cell survival under adverse conditions and inhibit development of programmed cell death. It was shown, that the level of HSP70 increases in cardiomyocytes and brain cells in response to ischemia, that was connected with cardioprotective and neuroprotective effects. Besides, in recent years, clinical studies of HSP70 have demonstrated elevated level of HSP70 in peripheral blood lymphocytes in groups of patients with ischemic stroke and myocardial infarction. This review indicates that HSP70 can serve as a target for developing new approaches to diagnostics and therapy of cardiovascular and cerebrovascular diseases.

Keywords: Heat shock proteins, ischemic stroke, myocardial infarction, atherosclerosis, immunomodulatory activities, cerebral ischemia.

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[1]
Gusev EI, Skvortsova VI. Ishemiya golovnogo mozga 2001; 7: 164.
[2]
Ferrari R. Healthy versus sick myocites: metabolism, structure and function. Eur Heart J 2002; 4: G1-G12.
[3]
Macario AJ, Conway de Macario E. Sick chaperones, cellular stress, and disease. N Engl J Med 2005; 353(14): 1489-501.
[4]
Lee Y, Gustafsson AB. Role of apoptosis in cardiovascular disease. Apoptosis 2009; 14(4): 536-48.
[5]
Broughton B, Reutens D, Sobey C. Apoptotic mechanism after cerebral ischemia. Stroke 2009; 40: e331-9.
[6]
Ritossa F. A new puffing pattern induced and temperature shock and DNP in Drosophilia. Experimentia 1962; 18: 571-3.
[7]
Tissières A, Mitchell HK, Tracy UM. Protein synthesis in salivary glands of Drosophila melanogaster: relation to chromosome puffs. J Mol Biol 1974; 84(3): 389-98.
[8]
Hartl FU, Hayer-Hartl M. Molecular chaperones in the cytosol: from nascent chain to folded protein. Science 2002; 295(5561): 1852-8.
[9]
Joly AL, Wettstein G, Mignot G, Ghiringhelli F, Garrido C. Dual role of heat shock proteins as regulators of apoptosis and innate immunity. J Innate Immun 2010; 2(3): 238-47.
[10]
Henderson B, Pockley AG. Molecular chaperones and protein-folding catalysts as intercellular signaling regulators in immunity and inflammation. J Leukoc Biol 2010; 88(3): 445-62.
[11]
Takeda K, Akira S. Toll-like receptors in innate immunity. Int Immunol 2005; 17(1): 1-14.
[12]
Mambula SS, Stevenson MA, Ogawa K, Calderwood SK. Mechanisms for Hsp70 secretion: crossing membranes without a leader. Methods 2007; 43(3): 168-75.
[13]
Hunter-Lavin C, Davies EL, Bacelar MMFVG, Marshall MJ, Andrew SM, Williams JH. Hsp70 release from peripheral blood mononuclear cells. Biochem Biophys Res Commun 2004; 324(2): 511-7.
[14]
Satoh M, Shimoda Y, Akatsu T, Ishikawa Y, Minami Y, Nakamura M. Elevated circulating levels of heat shock protein 70 are related to systemic inflammatory reaction through monocyte Toll signal in patients with heart failure after acute myocardial infarction. Eur J Heart Fail 2006; 8(8): 810-5.
[15]
Xu Q. Role of heat shock proteins in atherosclerosis. Arterioscler Thromb Vasc Biol 2002; 22(10): 1547-59.
[16]
Chistiakov DA, Orekhov AN, Bobryshev YV. Effects of shear stress on endothelial cells: go with the flow. Acta Physiol (Oxf) 2017; 219(2): 382-408.
[17]
Pockley AG, Shepherd J, Corton JM. Detection of heat shock protein 70 (Hsp70) and anti-Hsp70 antibodies in the serum of normal individuals. Immunol Invest 1998; 27(6): 367-77.
[18]
Pockley AG, Georgiades A, Thulin T, de Faire U, Frostegård J. Serum heat shock protein 70 levels predict the development of atherosclerosis in subjects with established hypertension. Hypertension 2003; 42(3): 235-8.
[19]
Zhu J, Quyyumi AA, Wu H, et al. Increased serum levels of heat shock protein 70 are associated with low risk of coronary artery disease. Arterioscler Thromb Vasc Biol 2003; 23(6): 1055-9.
[20]
Terry DF, McCormick M, Andersen S, et al. Cardiovascular disease delay in centenarian offspring: role of heat shock proteins. Ann N Y Acad Sci 2004; 1019: 502-5.
[21]
Terry DF, Wilcox MA, McCormick MA, Perls TT. Cardiovascular disease delay in centenarian offspring. J Gerontol A Biol Sci Med Sci 2004; 59(4): 385-9.
[22]
Zhang X, Xu Z, Zhou L, et al. Plasma levels of Hsp70 and anti-Hsp70 antibody predict risk of acute coronary syndrome. Cell Stress Chaperones 2010; 15(5): 675-86.
[23]
Berberian PA, Myers W, Tytell M, Challa V, Bond MG. Immunohistochemical localization of heat shock protein-70 in normal-appearing and atherosclerotic specimens of human arteries. Am J Pathol 1990; 136(1): 71-80.
[24]
Bobryshev YV, Lord RS. Expression of heat shock protein-70 by dendritic cells in the arterial intima and its potential significance in atherogenesis. J Vasc Surg 2002; 35(2): 368-75.
[25]
Okada M, Hasebe N, Aizawa Y, Izawa K, Kawabe J, Kikuchi K. Thermal treatment attenuates neointimal thickening with enhanced expression of heat-shock protein 72 and suppression of oxidative stress. Circulation 2004; 109(14): 1763-8.
[26]
Theriault JR, Mambula SS, Sawamura T, Stevenson MA, Calderwood SK. Extracellular HSP70 binding to surface receptors present on antigen presenting cells and endothelial/epithelial cells. 2005; 579: 1951-60.
[27]
Wick G, Knoflach M, Xu Q. Autoimmune and inflammatory mechanisms in atherosclerosis. Annu Rev Immunol 2004; 22: 361-403.
[28]
Tanimoto T, Parseghian MH, Nakahara T, et al. Cardioprotective effects of HSP72 administration on ischemia‐reperfusion injury. J Am Coll Cardiol 2017; 70(12): 1479-92.
[29]
Song Y-J, Zhong C-B, Wang X-B. Heat shock protein 70: A promising therapeutic target formyocardial ischemia–reperfusion injury. J Cell Physiol 2019; 234(2): 1190-207.
[30]
Suzuki K, Sawa Y, Kagisaki K, et al. Reduction in myocardial apoptosis associated with overexpression of heat shock protein 70. Basic Res Cardiol 2000; 95(5): 397-403.
[31]
Lüss H, Schäfers M, Neumann J, et al. Biochemical mechanisms of hibernation and stunning in the human heart. Cardiovasc Res 2002; 56(3): 411-21.
[32]
Sun JZ, Tang XL, Knowlton AA, Park SW, Qiu Y, Bolli R. Late preconditioning against myocardial stunning. An endogenous protective mechanism that confers resistance to postischemic dysfunction 24 h after brief ischemia in conscious pigs. J Clin Invest 1995; 95(1): 388-403.
[33]
Dybdahl B, Slørdahl SA, Waage A, Kierulf P, Espevik T, Sundan A. Myocardial ischaemia and the inflammatory response: release of heat shock protein 70 after myocardial infarction. Heart 2005; 91(3): 299-304.
[34]
Jenei ZM, Gombos T, Förhécz Z, et al. Elevated extracellular HSP70 (HSPA1A) level as an independent prognostic marker of mortality in patients with heart failure. Cell Stress Chaperones 2013; 18(6): 809-13.
[35]
Konstantinova EV, Khomyakova NF, Konstantinova NA, Podkolzina AV, Sapozhnikov AM. Relationship between apoptosis and expression of heat shock proteins in peripheral blood lymphocytes of patients with myocardial infarction. Bull Exp Biol Med 2011; 150(6): 682-4.
[36]
Giffard RG, Yenari MA. Many mechanisms for hsp70 protection from cerebral ischemia. J Neurosurg Anesthesiol 2004; 16(1): 53-61.
[37]
Popp A, Jaenisch N, Witte OW, Frahm C. Identification of ischemic regions in a rat model of stroke. PLoS One 2009; 4(3)e4764
[38]
Rajdev S, Hara K, Kokubo Y, et al. Mice overexpressing rat heat shock protein 70 are protected against cerebral infarction. Ann Neurol 2000; 47(6): 782-91.
[39]
Tsuchiya D, Hong S, Matsumori Y, et al. Overexpression of rat heat shock protein 70 reduces neuronal injury after transient focal ischemia, transient global ischemia, or kainic acid-induced seizures. Neurosurgery 2003; 53(5): 1179-87.
[40]
Lee SH, Kim M, Yoon BW, et al. Targeted hsp70.1 disruption increases infarction volume after focal cerebral ischemia in mice. Stroke 2001; 32(12): 2905-12.
[41]
Doeppner TR, Nagel F, Dietz GP, et al. TAT-Hsp70-mediated neuroprotection and increased survival of neuronal precursor cells after focal cerebral ischemia in mice. J Cereb Blood Flow Metab 2009; 29(6): 1187-96.
[42]
Mohammadi F, Nezafat N, Negahdaripour M, et al. Neuroprotective Effects of Heat Shock Protein70. CNS Neurol Disord Drug Targets 2018; 17(10): 736-42. E-pub Ahead of Print
[43]
Shevtsov MA, Nikolaev BP, Yakovleva LY, et al. Neurotherapeutic activity of the recombinant heat shock protein Hsp70 in a model of focal cerebral ischemia in rats. Drug Des Devel Ther 2014; 8: 639-50.
[44]
Kelly S, Zhang ZJ, Zhao H, et al. Gene transfer of HSP72 protects cornu ammonis 1 region of the hippocampus neurons from global ischemia: influence of Bcl-2. Ann Neurol 2002; 52(2): 160-7.
[45]
Giffard RG, Xu L, Zhao H, et al. Chaperones, protein aggregation, and brain protection from hypoxic/ischemic injury. J Exp Biol 2004; 207(Pt 18): 3213-20.
[46]
Zheng Z, Kim JY, Ma H, Lee JE, Yenari MA. Anti-inflammatory effects of the 70 kDa heat shock protein in experimental stroke. J Cereb Blood Flow Metab 2008; 28(1): 53-63.
[47]
Lee JE, Kim YJ, Kim JY, Lee WT, Yenari MA, Giffard RG. The 70 kDa heat shock protein suppresses matrix metalloproteinases in astrocytes. Neuroreport 2004; 15(3): 499-502.
[48]
Weinstein PR, Hong S, Sharp FR. Molecular identification of the ischemic penumbra. Stroke 2004; 35(11)(Suppl. 1): 2666-70.
[49]
Zhan X, Kim C, Sharp FR. Very brief focal ischemia simulating transient ischemic attacks (TIAs) can injure brain and induce Hsp70 protein. Brain Res 2008; 1234: 183-97.
[50]
Tytell M, Greenberg SG, Lasek RJ. Heat shock-like protein is transferred from glia to axon. Brain Res 1986; 363(1): 161-4.
[51]
Hightower LE, Guidon PT Jr. Selective release from cultured mammalian cells of heat-shock (stress) proteins that resemble glia-axon transfer proteins. J Cell Physiol 1989; 138(2): 257-66.
[52]
Jin X, Xiao C, Tanguay RM, et al. Correlation of lymphocyte heat shock protein 70 levels with neurologic deficits in elderly patients with cerebral infarction. Am J Med 2004; 117(6): 406-11.
[53]
Gromadzka G, Zielińska J, Ryglewicz D, Fiszer U, Członkowska A. Elevated levels of anti-heat shock protein antibodies in patients with cerebral ischemia. Cerebrovasc Dis 2001; 12(3): 235-9.

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