АКТУАЛЬНЫЕ АСПЕКТЫ В МЕХАНИЗМАХ АКТИВАЦИИ ТУЧНЫХ КЛЕТОК ПРИ ИШЕМИЧЕСКОМ И РЕПЕРФУЗИОННОМ ПОВРЕЖДЕНИИ

DOI: https://doi.org/10.29296/24999490-2019-06-03

Т.А. Ягудин(1, 2), В.Ш. Ишметов(1), доктор медицинских наук, профессор, В.В. Плечев(1), доктор медицинских наук, профессор, В.Н. Павлов(1), доктор медицинских наук, профессор, Лиу Хонг-Ю(2), доктор медицинских наук, профессор 1-ФГБОУ ВО «Башкирский государственный медицинский университет» Минздрава России, Российская Федерация, 450008, Республика Башкортостан, Уфа, ул. Ленина, д. 3; 2-Харбинский медицинский университет, Китай, 150081, провинция Хэйлунцзян, Харбин, район Наньган, ул. Баотиен 157 E-mail: [email protected]

Проанализирована литература о механизмах активации тучных клеток (ТК), которые являются регуляторными клетками, составляют важную часть иммунной системы и входят в первую линию защиты против различных патологических агентов. Доказана важная роль ТК при анафилактической реакции и аллергии, но появились данные, согласно которым тучные клетки принимают участие в более широком спектре патологий. Ишемическое/реперфузионное (И/Р) повреждение вызывает воспалительную реакцию и запускает программу повреждения/восстановления тканей, известную как иммунная регуляция. Уникальное расположение ТК вокруг микроциркуляторных сосудов делает их потенциально первым звеном в ответ на раннее и специфическое И/Р-повреждение посредством высвобождения медиаторов ТК. Многофункциональность и гетерогенность – отличительные признаки ТК, приобретенные в результате разных адаптаций в ходе филогенеза. Таким образом, это важные функции ТК, способные различаться в зависимости от тканей, в которых они находятся; различные эффекты, присущие ТК во время И/Р, являются актуальным сегодня вопросом. Представлен анализ литературы о роли ТК при И/Р-повреждении миокарда, мозга, почек, внутренних органов или систем. Понимание механизмов и роли ТК при И/Р-повреждении поможет в развитии терапевтических стратегий, нацеленных на защиту от специфического повреждения.
Ключевые слова: 
тучные клетки, дегрануляция
Для цитирования: 
Ягудин Т.А., Ишметов В.Ш., Плечев В.В., Павлов В.Н., Хонг-Ю Лиу АКТУАЛЬНЫЕ АСПЕКТЫ В МЕХАНИЗМАХ АКТИВАЦИИ ТУЧНЫХ КЛЕТОК ПРИ ИШЕМИЧЕСКОМ И РЕПЕРФУЗИОННОМ ПОВРЕЖДЕНИИ. Молекулярная медицина, 2019; (6): -https://doi.org/10.29296/24999490-2019-06-03
Список литературы: 
  1. Castells M. Diagnosis and management of anaphylaxis in precision medicine. J. Allergy Clin. Immunol. 2017; 140: 321e33. https://doi.org/10.1016/j.jaci.2017.06.012
  2. Bulfone-Paus S., Nilsson G., Draber P., Blank U., LeviSchaffer F. Positive and negative signals in mast cell activation. Trends Immunol. 2017; 38: 657e67 . https://doi.org/10.1016/j.it.2017.01.008
  3. Ali H. Emerging roles for MAS-related G protein-coupled receptor-X2 in host defense peptide, opioid, and neuropeptide-mediated inflammatory reactions. Adv Immunol 2017; 136: 123e62. https://doi.org/10.1016/bs.ai.2017.06.002
  4. Finkelman F.D., Khodoun M.V., Strait R. Human IgEindependent systemic anaphylaxis. J. Allergy Clin. Immunol. 2016; 137: 1674e80. https://doi.org/10.1016/j.jaci.2016.02.015
  5. Reber L.L., Hernandez J.D., Galli S.J. The pathophysiology of anaphylaxis. J. Allergy Clin. Immunol. 2017; 140: 335e48. https://doi.org/10.1016/j.jaci.2017.06.003
  6. Gaudenzio N., Sibilano R., Marichal T. Different activation signals induce distinct mast cell degranulation strategies. J. Clin. Invest. 2016; 126: 3981e98. https://doi.org/10.1172/JCI85538.
  7. Uyttebroek A.P., Sabato V., Leysen J., Bridts C.H., De Clerck L.S., Ebo D.G. Flowcytometric diagnosis of atracurium-induced anaphylaxis. Allergy. 2014; 69: 1324e32. https://doi.org/10.1111/all.12468
  8. Karhausen J., Abraham S.N. How mast cells make decisions. J. Clin. Invest. 2016; 126: 3735e8. https://doi.org/10.1172/JCI90361
  9. Uyttebroek A.P., Sabato V., Bridts C.H., De Clerck L.S., Ebo D.G. Immunoglobulin E antibodies to atracurium: a new diagnostic tool? Clin. Exp. Allergy. 2015; 45: 485e7. https://doi.org/10.1111/cea.12448
  10. Gouel-Cheron A., de Chaisemartin L., Jonsson F., NicaiseRoland P., Granger V., Sabahov A. Low end-tidal CO2 as a real-time severity marker of intra-anaesthetic acute hypersensitivity reactions. Br. J. Anaesth. 2017; 119: 908e17 https://doi.org/10.1093/bja/aex260
  11. Lurie K.G., Nemergut E.C., Yannopoulos D., Sweeney M. The physiology of cardiopulmonary resuscitation. Anesth Analg. 2016; 122: 767e83 https://doi.org/10.1213/ANE.0000000000000926
  12. Schulkes K.J.G., Van den Elzen M.T., Hack E.C., Otten H.G., Bruijnzeel-Koomen C., Knulst A.C. Clinical similarities among bradykinin-mediated and mast cell-mediated subtypes of non-hereditary angioedema: a retrospective study. Clin. Transl. Allergy. 2015; 5: 5. https://doi.org/10.1186/s13601-015-0049-8
  13. Chen Y.C., Chang Y.C., Chang H.A. Differential Ca2+ mobilization and mast cell degranulation by FcεRI-and GPCR-mediated signaling [J]. Cell calcium. 2017; 67: 31–9. https://doi.org/10.1016/j.ceca.2017.08.002
  14. Peralta C.A., Jimenezcastro M.B., Graciasancho J. Hepatic ischemia and reperfusion injury: effects on the liver sinusoidal milieu. [J]. J. of Hepatology. 2013; 59 (5): 1094–106. https://doi.org/10.1172/FCI856.
  15. Gersch C., Dewald O., Zoerlein M. Mast cells and macrophages in normal C57/BL/6 mice [J]. Histochemistry and Cell Biology. 2002; 118 (1): 41–9. https://doi.org/10.1177/YGYI8576.
  16. Vicencio J.M., Yellon D.M., Sivaraman V. Plasma exosomes protect the myocardium from ischemia-reperfusion injury [J]. J. of the American College of Cardiology. 2015; 65 (15): 1525–36. https://doi.org/10.1172/U855566.
  17. Ingason A.B., Mechmet F., Atacho D.A.M. Distribution of mast cells within the mouse heart and its dependency on Mitf [J]. Molecular immunology. 2019; 105: 9–15. https://doi.org/10.11111/JCI54476545.
  18. Caughey G.H. Mast cell proteases as pharmacological targets [J]. Eur. J. of pharmacology. 2016, 778: 44–55. https://doi.org/10.1038/s41598-017-11985-6
  19. Rothmeier A.S., Ruf W. Protease-activated receptor 2 signaling in inflammation [C] Seminars in immunopathology. Springer-Verlag. 2012; 34 (1): 133–49. https://doi.org/10.4103/0366-6999.241557
  20. Nelissen S., Lemmens E., Geurts N. The role of mast cells in neuroinflammation [J]. Acta Neuropathologica. 2013; 125 (5): 637–50. https://doi.org/10.1021/acsami.7b05669
  21. Frieri M., Kumar K., Boutin A. Role of mast cells in trauma and neuroinflammation in allergy immunology [J]. Annals of Allergy Asthma & Immunology. 2015; 115 (3): 172–7. https://doi.org/10.1061/aust.77880
  22. Biran V., Cochois V., Karroubi A. Stroke induces histamine accumulation and mast cell degranulation in the neonatal rat brain [J]. Brain Pathology. 2008; 18 (1): 1–9. https://doi.org/10.21470/1678-97412017-0099
  23. Cadenas S. ROS and redox signaling in myocardial ischemia-reperfusion injury and cardioprotection [J]. Free Radical Biology and Medicine. 2018. https://doi.org/10.1016/j.freeradbiomed.2018.01.024
  24. Tejada T., Tan L., Torres R.A. IGF-1 degradation by mouse mast cell protease promotes cell death and adverse cardiac remodeling days after a myocardial infarction [J]. Proceedings of the National Academy of Sciences of the United States of America. 2016; 113 (25): 6949–54. https://doi.org/10.1073/pnas.1603127113
  25. Neumann F.J., Sousa-Uva M., Ahlsson A. 2018 ESC/EACTS guidelines on myocardial revascularization [J]. Kardiologia Polska (Polish Heart J.). 2018; 76 (12): 1585–664. https://doi.org/10.1093/eurheartj/ehy658
  26. Baines C.P. How and when do myocytes die during ischemia and reperfusion: the late phase. J. Cardiovasc Pharmacol Ther. 2011; 16 (3–4): 239–43. https://doi.org/10.1177/1074248411407769
  27. Marino A., Sakamoto T., Robador P.A. S1P receptor 1-Mediated Anti– Renin-Angiotensin System Cardioprotection: Pivotal Role of Mast Cell Aldehyde Dehydrogenase Type 2 [J]. J. of Pharmacology and Experimental Therapeutics. 2017; 362 (2): 230–42. https://doi.org/10.1124/jpet.117.241976
  28. Marino A., Levi R. Salvaging the Ischemic Heart: Gi-Coupled Receptors in Mast Cells Activate a PKCE/ALDH2 Pathway Providing Anti-RAS Cardioprotection [J]. Current medicinal chemistry. 2018; 25 (34): 4416–31. https://doi.org/10.2174/0929867325666180214115127
  29. Wong A.M., Hodges H., Horsburgh K. Neural stem cell grafts reduce the extent of neuronal damage in a mouse model of global ischaemia [J]. Brain research. 2005; 1063 (2): 140–50. https://doi.org/10.1016/j.brainres.2005.09.049
  30. Zhao H., Alam A., Soo A.P. Ischemia-Reperfusion Injury Reduces Long Term Renal Graft Survival: Mechanism and Beyond [J]. EBioMedicine. 2018; 28: 31–42. https://doi.org/10.1016/j.ebiom.2018.01.025
  31. Basile D.P., Donohoe D., Roethe K. Renal ischemic injury results in permanent damage to peritubular capillaries and influences long-term function [J]. American J. of Physiology-Renal Physiology. 2018. https://doi.org/10.1152/ajprenal.2001.281.5.f887
  32. Danelli L., Madjene L.C., Madera-Salcedo I. Early Phase Mast Cell Activation Determines the Chronic Outcome of Renal Ischemia–Reperfusion Injury [J]. The J. of Immunology. 2017; 198 (6): 2374–82. https://doi.org/10.4049/jimmunol.1601282
  33. Binek A., Fernández-Jiménez R., Jorge I., Camafeita E., López J.A., Bagwan N. Proteomic footprint of myocardial ischemia/reperfusion injury: Longitudinal study of the at-risk and remote regions in the pig model. Scientific Reports. 2017; 7 (1). №12343. https://doi.org/10.1038/s41598-017-11985-5
  34. He Y., Zhang B., Chen Y., Jin Q., Wu J., Yan F. Image-Guided Hydrogen Gas Delivery for Protection from Myocardial Ischemia-Reperfusion Injury via Microbubbles. ACS Applied Materials and Interfaces. 2017; 9 (25): 21190–9. https://doi.org/10.1021/acsami.7b05346
  35. Zheng X.-H., Liu C.-P., Hao Z.-G., Wang Y.-F., Li X.-L. Protective effect and mechanistic evaluation of linalool against acute myocardial ischemia and reperfusion injury in rats. RSC Advances. 2017; 7 (55): 34473–81. https://doi.org/10.1039/c7ra00743d
  36. Zhao X., Zhang F., Wang Y. Proteomic analysis reveals Xuesaitong injection attenuates myocardial ischemia/reperfusion injury by elevating pyruvate dehydrogenase-mediated aerobic metabolism. Molecular BioSystems. 2017; 13 (8): 1504–11. https://doi.org/10.1039/c7mb00140a
  37. Yang G.-Z., Xue F.-S., Liu Y.-Y., Li H.-X., Liu Q., Liao X. Feasibility Analysis of Oxygen-Glucose Deprivation-Nutrition Resumption on H9c2 Cells in vitro Models of Myocardial Ischemia-Reperfusion Injury. Chinese Medical J. 2018; 131: 2277–86. https://doi.org/10.4103/0366-6999.241809
  38. Wang S., Liu C., Gong C., Li T., Zhao J., Xiao W. Alpha linolenic acid intake alleviates myocardial ischemia/reperfusion injury via the P2X7R/NF-κB signalling pathway. J. of Functional Foods. 2018; 49: 1–11. https://doi.org/10.1016/j.jff.2018.08.012
  39. Zhang S.-B., Liu T.-J., Pu G.-H., Li B.-Y., Gao X.-Z., Han X.-L. Suppression of Long Non-Coding RNA LINC00652 Restores Sevoflurane-Induced Cardioprotection Against Myocardial Ischemia-Reperfusion Injury by Targeting GLP-1R Through the cAMP/PKA Pathway in Mice. Cellular Physiology and Biochemistry. 2018; 49: 1476–91. https://doi.org/10.1159/000493450
  40. Luo C., Yuan D., Zhao W. Sevoflurane ameliorates intestinal ischemia-reperfusion-induced lung injury by inhibiting the synergistic action between mast cell activation and oxidative stress [J]. Molecular medicine reports. 2015; 12 (1): 1082–90. https://doi.org/10.1038/s41598-017-11985-98
  41. Zhao W., Zhou S., Yao W. Propofol prevents lung injury after intestinal ischemia–reperfusion by inhibiting the interaction between mast cell activation and oxidative stress [J]. Life sciences. 2014; 108 (2): 80–7. https://doi.org/10.4103/0366-6999
  42. Tong F., Luo L., Liu D. Effect of intervention in mast cell function before reperfusion on renal ischemia-reperfusion injury in rats [J]. Kidney and Blood Pressure Research. 2016; 41 (3): 335–44. https://doi.org/10.1021/acsami.7b05390
  43. Baba A., Tachi M., Ejima Y. Less contribution of mast cells to the progression of renal fibrosis in Rat kidneys with chronic renal failure [J]. Nephrology. 2017; 22 (2): 159–67. https://doi.org/10.1093/eurheartj/ehy697
  44. Danelli L., Madjene L.C., Madera-Salcedo I. Early Phase Mast Cell Activation Determines the Chronic Outcome of Renal Ischemia–Reperfusion Injury [J]. The J. of Immunology. 2017; 198 (6): 2374–82. https://doi.org/10.1039/c7mb0776
  45. Horie Y., Ishii H. Liver dysfunction elicited by gut ischemia-reperfusion [J]. Pathophysiology. 2001; 8 (1): 11–20. https://doi.org/10.1016/s0928-4680(01)00063-3
  46. Pierro A., Eaton S. Intestinal ischemia reperfusion injury and multisystem organ failure [J]. Seminars in Pediatric Surgery. 2004; 13 (1): 11–7. https://doi.org/10.1053/j.sempedsurg.2003.09.003
  47. Yang, C.-F. Clinical manifestations and basic mechanisms of myocardial ischemia/reperfusion injury. Tzu Chi Medical J. 2018; 30 (4): 209–15. https://doi.org/10.4103/tcmj.tcmj_33_18
  48. Geldi O., Kubat E., Ünal C.S., Canbaz S. Acetaminophen mitigates myocardial injury induced by lower extremity ischemia-reperfusion in rat model. Brazilian J. of Cardiovascular Surgery. 2018; 33 (3): 258–64. https://doi.org/10.21470/1678-97412017
  49. Jeddi S., Ghasemi A., Asgari A., Nezami-Asl A. Role of inducible nitric oxide synthase in myocardial ischemia-reperfusion injury in sleep-deprived rats. Sleep and Breathing. 2018; 22 (2): 353–9. https://doi.org/10.1007/s11325-017-1573
  50. Dahlin J.S., Hallgren J. Mast cell progenitors: origin, development and migration to tissues [J]. Molecular immunology. 2015; 63 (1): 9–17. https://doi.org/10.1093/eurheartj/976