We studied the effect of extracellular vesicular particles generated during apoptosis by macrophages of M0, M1 and M2 phenotypes on spontaneous and LPS-stimulated production of NO. The fractions of apoptotic bodies and apoptotic microvesicles were obtained in the primary cultures of peritoneal macrophages undergoing apoptosis. The effect of these microparticles on LPS-induced proinflammatory response of recipient macrophages critically depends on the initial phenotype of “donor” macrophages. Microvesicles and especially apoptotic bodies from M1 macrophages stimulate basal NO production. LPS stimulation of these macrophages preincubated with apoptotic bodies was not followed by further growth of NO production; in macrophages preincubated with microvesicles, LPS even suppressed NO production. Apoptotic microparticles obtained from M2 macrophages produced little effect on the basal production of NO. LPS stimulation of macrophages-recipients preincubated with microparticles from M2 macrophages did not enhance NO production. Incubation of macrophages with apoptotic microparticles induces the formation of endotoxic tolerance.
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Schwartz YS, Svistelnik AV. Functional phenotypes of macrophages and the M1-M2 polarization concept. Part I. Proinflammatory phenotype. Biochemistry (Moscow) 2012;77(3):246-260.
Schwartz YSh, Khoshchenko OM, Dushkin MI, Feofanova NA. Effects of cholesterol and nuclear hormone receptor agonists on the production of transforming growth factor-beta in macrophages. Bull. Exp. Biol. Med. 2009;148(3):406-409.
Akers JC, Gonda D, Kim R, Carter BS, Chen CC. Biogenesis of extracellular vesicles (EV): exosomes, microvesicles, retrovirus-like vesicles, and apoptotic bodies. J. Neurooncol. 2013;113(1):1-11.
Chang CC, McCormick CC, Lin AW, Dietert RR, Sung YJ. Inhibition of nitric oxide synthase gene expression in vivo and in vitro by repeated doses of endotoxin. Am. J. Physiol. 1996;271(4, Pt 1):G539-G548.
Chin BY, Petrache I, Choi AM, Choi ME. Transforming growth factor beta1 rescues serum deprivation-induced apoptosis via the mitogen-activated protein kinase (MAPK) pathway in macrophages. J. Biol. Chem. 1999;274(16):11,362-11,368.
Crescitelli R, Lässer C, Szabó TG, Kittel A, Eldh M, Dianzani I, Buzás EI, Lötvall J. Distinct RNA profiles in subpopulations of extracellular vesicles: apoptotic bodies, microvesicles and exosomes. J. Extracell. Vesicles. 2013;2. doi: https://doi.org/10.3402/jev.v2i0.20677.
Griess Reagent System Technical Bulletin TB229, Promega, 06/2005:1-7.
Dias MB, Almeida MC, Carnio EC, Branco LG. Role of nitric oxide in tolerance to lipopolysaccharide in mice. J. Appl. Physiol. 2005;98(4):1322-1327.
Leroyer AS, Isobe H, Lesèche G, Castier Y, Wassef M, Mallat Z, Binder BR, Tedgui A, Boulanger CM. Cellular origins and thrombogenic activity of microparticles isolated from human atherosclerotic plaques. J. Am. Coll. Cardiol. 2007;49(7):772-777.
Mills CD. M1 and M2 macrophages: oracles of health and disease. Crit. Rev. Immunol. 2012;32(6):463-488.
Nomura S, Suzuki M, Katsura K, Xie GL, Miyazaki Y, Miyake T, Kido H, Kagawa H, Fukuhara S. Platelet-derived microparticles may influence the development of atherosclerosis in diabetes mellitus. Atherosclerosis 1995;116(2):235-240.
Robbins PD, Morelli AE. Regulation of immune responses by extracellular vesicles. Nat. Rev. Immunol. 2014;14(3):195-208.
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Translated from Byulleten’ Eksperimental’noi Biologii i Meditsiny, Vol. 165, No. 4, pp. 443-446, April, 2018
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Schwartz, Y.S., Dolganova, O.M., Rudina, M.I. et al. Influence of Apoptotic Bodies and Apoptotic Microvesicles on NO Production in Macrophages. Bull Exp Biol Med 165, 453–456 (2018). https://doi.org/10.1007/s10517-018-4192-9
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DOI: https://doi.org/10.1007/s10517-018-4192-9