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Разрушение и перестройка внеклеточного матрикса в патогенезе острой очаговой ишемии головного мозга
Разрушение и перестройка внеклеточного матрикса в патогенезе острой очаговой ишемии головного мозга
Константинова Е.В., Шурдумова М.Х. Разрушение и перестройка внеклеточного матрикса в патогенезе острой очаговой ишемии головного мозга. Consilium Medicum. 2015; 17 (12): 50–54. DOI:10.26442/2075-1753_2015.12.50-54
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Аннотация
В обзоре представлен современный взгляд на участие матриксных металлопротеиназ (ММП) в патогенезе ишемического инсульта. Охарактеризованы основные типы ММП, функция которых связана с обменом соединительнотканного матрикса в норме и при патологии. Описана роль ММП при развитии атеротромбоза. Показано, что одним из факторов, приводящих к повреждению атеросклеротической бляшки, является повышение уровня ММП, особенно выраженное в наиболее уязвимой области бляшки – плечевой. С другой стороны, выявлены свойства ММП – укреплять покрышку атеросклеротической бляшки. Представлено, что уровень циркулирующей в крови ММП-9 ассоциируется с прогрессированием атеросклероза и риском сердечно-сосудистого события. Обобщены результаты экспериментальных и клинических исследований по изучению роли ММП-9 при острой ишемии головного мозга. Показано нарастание ММП-9 в первые часы острой ишемии в очаге повреждения, а также в сыворотке периферической крови. Представлены данные о разнонаправленном действии ММП-9 в патогенезе острой фокальной ишемии головного мозга. Учитывая доказанное влияние уровня ММП-9 на формирование очага ишемического повреждения, описаны группы препаратов, действующих на уровень ММП-9.
Ключевые слова: ишемический инсульт, матриксные металлопротеиназы, атеросклероз.
Ключевые слова: ишемический инсульт, матриксные металлопротеиназы, атеросклероз.
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The review presents the current view of the part of matrix metalloproteinases (MMPs) in the pathogenesis of ischemic stroke. It describes the main types of MMP, the function of which is related to the exchange of connective tissue matrix in normal and pathological conditions. Describe the role of MMPs in the development of atherothrombosis. It is shown that one of the factors that lead to the damage of plaque, is to increase the IMF, particularly pronounced in the most vulnerable areas of plaque – the shoulder. On the other hand, revealed the properties of MMP strengthen tire atherosclerosis plaque. Transmitted by the level of circulating MMP-9 is associated with the progression of atherosclerosis and the risk of cardiovascular events. The results of experimental and clinical studies on the role of MMP-9 in acute cerebral ischemia are generalized. Shown to increase MMP-9 in the first hours of acute ischemia in the lesion and in peripheral blood serum. Presents the multidirectional action of MMP-9 in the pathogenesis of acute focal cerebral ischemia. Described the group of drugs acting on the level of MMP-9.
Key words: ischemic stroke, matrix metalloproteinases, atherosclerosis.
Key words: ischemic stroke, matrix metalloproteinases, atherosclerosis.
Полный текст
Список литературы
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50. Miyazaki S, Kasai T, Miyauchi K et al. Changes of matrix metalloproteinase-9 level is associated with left ventricular remodeling following acute myocardial infarction among patients treated with trandolapril, valsartan or both. Circulation 2010; 74: 1158–64.
51. Hayashidani S, Tsutsui H, Shiomi T et al. Fluvastatin, a 3-hydroxyl-3-methylglutaryl coenzyme A reductase inhibitor, attenuates left ventricular remodelling and failure after experimental myocardial infarction. Circulation 2002; 105: 868–73.
52. Luan Z, Chase AJ, Newby AC. Statins inhibit secretion of metalloproteinases-1, -2, -3, and -9 from vascular smooth muscle cells and macrophages. Arterioscler Thromb Vas Biol 2003; 23: 769–75.
2. Peeters W, Hellings WE, de Kleijn DPV et al. Carotid atherosclerotic plaques stabilize after stroke insights into the natural process of atherosclerotic plaque stabilization. Arterioscler Thromb Vasc Biol 2009; 29: 128–33.
3. Redgrave JN, Lovett JK, Gallagher PJ. Histological assessment of 526 symptomatic carotid plaques in relation to the nature and timing of ischemic symptoms: the Oxford plaque study. Circulation 2006; 113: 2320–8.
4. Gasche Y, Soccal PM, Kanemitsu M. Matrix metalloproteinases and diseases of the central nervous system with a special emphasis on ischemic brain. Front Biosci 2006; 11: 1289–301.
5. Murphy G, Nagase H. Progress in matrix metalloproteinase research. Mol Aspects Med 2008; 29: 290–308.
6. Nagase H, Visse R, Murphy G. Structure and function of matrix metalloproteinases and TIMPs. Сardiovasc Res 2006; 69: 562–73.
7. Spinale FG. Myocardial matrix remodeling and the matrix metalloproteinases: influence on cardiac form and function. Physiol Rev 2007; 87: 1285–342.
8. Galis ZS, Sukhova GK, Lark MW. Increased expression of matrix metalloproteinases and matrix degrading activity in vulnerable regions of human atherosclerotic plaques. J Clin Invest 1994; 94: 2493–503.
9. Newby AC. Metalloproteinase expression in monocytes and macrophages and its relationship to atherosclerotic plaque instability. Arterioscler Thromb Vasc Biol 2008; 28: 2108–14.
10. Dollery CM, Libby P. Atherosclerosis and proteinase activation. Cardiovasc Res 2006; 69: 625–35.
11. Johnson C, Galis ZS. Matrix metalloproteinase-2 and -9 differentially regulate smooth muscle cell migration and cell-mediated collagen organization. Arterioscler Thromb Vase Biol 2004; 24: 54–60.
12. Newby AC. Dual role of matrix metalloproteinases (matrixins) in intimal thickening and atherosclerotic plaque rupture. Physiol Rev 2005: 85: 1–31.
13. Abdelnaseer M, Elfayomi N, Esmail EH et al. Relationship between matrix metalloproteinase-9 and common carotid artery intima media thickness. Neurol Sci 2015; Aug 30.
14. Stuijter JP, Pulskens WP, Schoneveld AH et al. Matrix metalloproteinase 2 is associated with stable and matrix metalloproteinases 8 and 9 with vulnerable carotid atherosclerotic lesions a study in human endarterectomy specimen pointing to a role for different extracellular matrix metalloproteinases inducer glycosylation forms. Stroke 2006; 37: 235–9.
15. Abelleira S, Bevan S, Markus H. Matrix metalloproteinases. J Med Genet 2006; 43: 897–901.
16. Kaplan RC, Smith NL, Zucker S. Matrix metalloproteinase-3 (MMP3) and MMP9 genes and risk of myocardial infarction, ischemic stroke, and hemorrhagic stroke. Atherosclerosis 2008; 201: 130–7.
17. Eldrup N, Gronholdt ML, Sillesen H. Elevated matrix metalloproteinase-9 associated with stroke or cardiovascular death in patients with carotid stenosis. Circulation 2006; 114: 1847–54.
18. Welsh P, Whincup PH, Papacosta O. Serum matrix metalloproteinase-9 and coronary heart disease: a prospective study in middle-aged men. QJM 2008; 101: 785–91.
19. Kopitsa N.P., Belaia N.V., Titarenko N.V. Rol' matriksnykh metalloproteinaz v patogeneze postinfarktnogo remodelirovaniia levogo zheludochka. Mezhdunar. med. zhurn. 2010; 4: 55–58. [in Russian]
20. Cunningham LA, Wetzel M, Rosenberg GA. Multiple roles for MMPs and TIMPs in cerebral ischemia. Glia 2005; 50: 329–39.
21. Rosell A, Ortega-Aznar A. Alvarez-Sabin J et al. Increased brain expression of Matrix Metalloproteinase-9 after ischemic and hemorrhagic human stroke. Stroke 2006; 37: 1399–406.
22. Egashira Y, Zhao H, Hua Y et al. White Matter Injury After Subarachnoid Hemorrhage: Role of Blood-Brain Barrier Disruption and Matrix Metalloproteinase-9. Stroke 2015; 46 (10): 2909–5.
23. Cadenas I, Ribo M, Molina CA et al. Increased brain expression of matrix metalloproteinase-9 after ischemic and hemorrhagic human stroke. Stroke 2006; 37: 1399–406.
24. Zhao BQ, Ikeda Y, Ihara H et al. Essential role of endogenous tissue plasminogen activator through matrix metalloproteinase 9 induction and expression on heparin-produced cerebral hemorrhage after cerebral ischemia in mice. Blood 2004; 103: 2610–6.
25. Rosell A, Cuadrado E, Ortega-Aznar A. Mmp-9-positive neutrophil infiltration is associated to blood-brain barrier breakdown and basal lamina type iv collagen degradation during hemorrhagic transformation after human ischemic stroke. Stroke 2008; 39: 1121–6.
26. Romanic AM, White RF, Arleth AJ et al. Matrix metalloproteinase expression increases after cerebral focal ischemia in rats: Inhibition of matrix metalloproteinase-9 reduces infarct size. Stroke 1998; 5: 1020–30.
27. Planas AM, Sole S, Justicia C. Expression and activation of matrix metalloproteinase-2 and-9 in rat brain after transient focal cerebral ischemia. Neurobiol Dis 2001; 8: 834–46.
28. Koh SH, Chang DI, Kim HT et al. Effect of 3-aminobenzamide, parp inhibitor, on matrix metalloproteinase-9 level in plasma and brain of ischemic stroke model. Toxicology 2005; 214: 131–9.
29. Park KP, Rossel A, Foerch C et al. Plasma and brain matrix metalloproteinase-9 after acute focal cerebral ischemia in rats. Stroke 2009; 40 (8): 2836–42.
30. Asahi M, Asahi K, Jung JC et al. Role for matrix metalloproteinase 9 after focal cerebral ischemia: effects of gene knockout and enzyme inhibition with BB-94. J Cereb Blood Flow Metab 2000; 20: 1681–9.
31. Asahi M, Wang X, Mori T et al. Effects of matrix metalloproteinase-9 gene knockout on the proteolysis of blood-brain barrier and white matter components after cerebral ischemia. J Neurosci 2001; 21: 7724–32.
32. Gu Z, Kaul M, Yan B et al. S-nitrosylation of matrix metalloproteinases: Signaling pathway to neuronal cell death. Science 2002; 297: 1186–90.
33. Lee SR, Lo EH. Induction of caspase-mediated cell death by matrix metalloproteinases in cerebral endothelial cells after hypoxia-reoxygen-ation. J Cereb Blood Flow Metab 2004; 24: 720–7.
34. Copin JC, Merlani P, Sugawara Т et al. Delayed matrix metalloproteinase inhibition reduces intracerebral hemorrhage after embolic stroke in rats. Exp Neurol 2008; 213: 196–201.
35. Liu XS, Chopp M, Zhang RL. Angiopoietin 2 mediates the differentiation and migration of neural progenitor cells in the subventricular zone after stroke. J Biol Chem 2009; 284 (34): 22680–9.
36. Lee SR, Kim HY, Rogowska J et al. Involvement of matrix metalloproteinase in neuroblast cell migration from the subventricular zone after stroke. J Neurosci 2006; 26: 3491–5.
37. Rosenberg GA. Matrix metalloproteinases and their multiple roles in neurodegenerative diseases. Lancet Neurol 2009: 8: 205–16.
38. Montaner J, Alvarez-Sabin J, Molina CA et al. Matrix metalloproteinase expression is related to hemorrhagic transformation after cardioembolic stroke. Stroke 2001; 32: 2762–7.
39. Montaner J, Rovira A, Molina CA et al. Plasmatic level of neuroinflammatory markers predict the extent of diffusion-weighted image lesions in hyperacute stroke. J Cereb Blood Flow Metab 2003; 23: 1403–7.
40. Horstmann S, Kalb P, Koziol J et al. Profiles of matrix metalloproteinases, their inhibitors, and laminin in stroke patients: Influence of different therapies. Stroke 2003; 34: 2165–70.
41. Shamalov N.A., Skvortsova V.I., Ramazanov G.R. i dr. Komp'iuterno-tomograficheskie i biokhimicheskie prediktory iskhodov tromboliticheskoi terapii u patsientov s ishemicheskim insul'tom. Zhurn. nevrologii i psikhiatrii im. S.S.Korsakova. 2010; 4: 21–8. [in Russian]
42. Coussens LM, Fingleton B, Matrisian LM. Matrix metalloproteinase inhibitors and cancer: trials and tribulations. Science 2002; 295: 2387–92.
43. Gusev E.I., Konovalov A.N., Skvortsova V.I., Gekht A.B. Nevrologiia: Natsional'noe rukovodstvo. M.: GEOTAR-Media, 2009; s. 592–615. [in Russian]
44. Guidelines for management of ischaemic stroke and transient ischaemic attack 2008. Cerebrovasc Dis 2008; 25 (5): 457–507.
45. Suzuki Y. Role of tissue-type plasminogen activator in ischemic stroke. J Pharmacol Sci 2010; 113: 203–7.
46. Suzuki Y, Nagai N, Umemura K et al. Stromelysin-1 (MMP-3) is critical for intracranial bleeding after t-PA treatment of stroke in mice. J Thromb Haemost 2007; 5: 1732–9.
47. Hosomi N, Nishiyama A, Ban CR et al. Angiotensin type 1 receptor blockage improves ischemic injury following transient focal cerebral ischemia. Neuroscience 2005; 134: 225–31.
48. Tanaka H, Takai S, Jin D et al. Inhibition of matrix metalloproteinase-9 activity by trandolapril after middle cerebral artery occlusion in rats. Hypertens Res 2007; 5: 469–75.
49. Liebetrau M, Burggraf D, Wunderlich N et al. ACE inhibition reduces activity of the plas-minogen/plasmin and MMP systems in the brain of spontaneous hypertensive stroke-prone rats. Neurosci Lett 2005; 376: 205–9.
50. Miyazaki S, Kasai T, Miyauchi K et al. Changes of matrix metalloproteinase-9 level is associated with left ventricular remodeling following acute myocardial infarction among patients treated with trandolapril, valsartan or both. Circulation 2010; 74: 1158–64.
51. Hayashidani S, Tsutsui H, Shiomi T et al. Fluvastatin, a 3-hydroxyl-3-methylglutaryl coenzyme A reductase inhibitor, attenuates left ventricular remodelling and failure after experimental myocardial infarction. Circulation 2002; 105: 868–73.
52. Luan Z, Chase AJ, Newby AC. Statins inhibit secretion of metalloproteinases-1, -2, -3, and -9 from vascular smooth muscle cells and macrophages. Arterioscler Thromb Vas Biol 2003; 23: 769–75.
2. Peeters W, Hellings WE, de Kleijn DPV et al. Carotid atherosclerotic plaques stabilize after stroke insights into the natural process of atherosclerotic plaque stabilization. Arterioscler Thromb Vasc Biol 2009; 29: 128–33.
3. Redgrave JN, Lovett JK, Gallagher PJ. Histological assessment of 526 symptomatic carotid plaques in relation to the nature and timing of ischemic symptoms: the Oxford plaque study. Circulation 2006; 113: 2320–8.
4. Gasche Y, Soccal PM, Kanemitsu M. Matrix metalloproteinases and diseases of the central nervous system with a special emphasis on ischemic brain. Front Biosci 2006; 11: 1289–301.
5. Murphy G, Nagase H. Progress in matrix metalloproteinase research. Mol Aspects Med 2008; 29: 290–308.
6. Nagase H, Visse R, Murphy G. Structure and function of matrix metalloproteinases and TIMPs. Сardiovasc Res 2006; 69: 562–73.
7. Spinale FG. Myocardial matrix remodeling and the matrix metalloproteinases: influence on cardiac form and function. Physiol Rev 2007; 87: 1285–342.
8. Galis ZS, Sukhova GK, Lark MW. Increased expression of matrix metalloproteinases and matrix degrading activity in vulnerable regions of human atherosclerotic plaques. J Clin Invest 1994; 94: 2493–503.
9. Newby AC. Metalloproteinase expression in monocytes and macrophages and its relationship to atherosclerotic plaque instability. Arterioscler Thromb Vasc Biol 2008; 28: 2108–14.
10. Dollery CM, Libby P. Atherosclerosis and proteinase activation. Cardiovasc Res 2006; 69: 625–35.
11. Johnson C, Galis ZS. Matrix metalloproteinase-2 and -9 differentially regulate smooth muscle cell migration and cell-mediated collagen organization. Arterioscler Thromb Vase Biol 2004; 24: 54–60.
12. Newby AC. Dual role of matrix metalloproteinases (matrixins) in intimal thickening and atherosclerotic plaque rupture. Physiol Rev 2005: 85: 1–31.
13. Abdelnaseer M, Elfayomi N, Esmail EH et al. Relationship between matrix metalloproteinase-9 and common carotid artery intima media thickness. Neurol Sci 2015; Aug 30.
14. Stuijter JP, Pulskens WP, Schoneveld AH et al. Matrix metalloproteinase 2 is associated with stable and matrix metalloproteinases 8 and 9 with vulnerable carotid atherosclerotic lesions a study in human endarterectomy specimen pointing to a role for different extracellular matrix metalloproteinases inducer glycosylation forms. Stroke 2006; 37: 235–9.
15. Abelleira S, Bevan S, Markus H. Matrix metalloproteinases. J Med Genet 2006; 43: 897–901.
16. Kaplan RC, Smith NL, Zucker S. Matrix metalloproteinase-3 (MMP3) and MMP9 genes and risk of myocardial infarction, ischemic stroke, and hemorrhagic stroke. Atherosclerosis 2008; 201: 130–7.
17. Eldrup N, Gronholdt ML, Sillesen H. Elevated matrix metalloproteinase-9 associated with stroke or cardiovascular death in patients with carotid stenosis. Circulation 2006; 114: 1847–54.
18. Welsh P, Whincup PH, Papacosta O. Serum matrix metalloproteinase-9 and coronary heart disease: a prospective study in middle-aged men. QJM 2008; 101: 785–91.
19. Копица Н.П., Белая Н.В., Титаренко Н.В. Роль матриксных металлопротеиназ в патогенезе постинфарктного ремоделирования левого желудочка. Междунар. мед. журн. 2010; 4: 55–58. / Kopitsa N.P., Belaia N.V., Titarenko N.V. Rol' matriksnykh metalloproteinaz v patogeneze postinfarktnogo remodelirovaniia levogo zheludochka. Mezhdunar. med. zhurn. 2010; 4: 55–58. [in Russian]
20. Cunningham LA, Wetzel M, Rosenberg GA. Multiple roles for MMPs and TIMPs in cerebral ischemia. Glia 2005; 50: 329–39.
21. Rosell A, Ortega-Aznar A. Alvarez-Sabin J et al. Increased brain expression of Matrix Metalloproteinase-9 after ischemic and hemorrhagic human stroke. Stroke 2006; 37: 1399–406.
22. Egashira Y, Zhao H, Hua Y et al. White Matter Injury After Subarachnoid Hemorrhage: Role of Blood-Brain Barrier Disruption and Matrix Metalloproteinase-9. Stroke 2015; 46 (10): 2909–5.
23. Cadenas I, Ribo M, Molina CA et al. Increased brain expression of matrix metalloproteinase-9 after ischemic and hemorrhagic human stroke. Stroke 2006; 37: 1399–406.
24. Zhao BQ, Ikeda Y, Ihara H et al. Essential role of endogenous tissue plasminogen activator through matrix metalloproteinase 9 induction and expression on heparin-produced cerebral hemorrhage after cerebral ischemia in mice. Blood 2004; 103: 2610–6.
25. Rosell A, Cuadrado E, Ortega-Aznar A. Mmp-9-positive neutrophil infiltration is associated to blood-brain barrier breakdown and basal lamina type iv collagen degradation during hemorrhagic transformation after human ischemic stroke. Stroke 2008; 39: 1121–6.
26. Romanic AM, White RF, Arleth AJ et al. Matrix metalloproteinase expression increases after cerebral focal ischemia in rats: Inhibition of matrix metalloproteinase-9 reduces infarct size. Stroke 1998; 5: 1020–30.
27. Planas AM, Sole S, Justicia C. Expression and activation of matrix metalloproteinase-2 and-9 in rat brain after transient focal cerebral ischemia. Neurobiol Dis 2001; 8: 834–46.
28. Koh SH, Chang DI, Kim HT et al. Effect of 3-aminobenzamide, parp inhibitor, on matrix metalloproteinase-9 level in plasma and brain of ischemic stroke model. Toxicology 2005; 214: 131–9.
29. Park KP, Rossel A, Foerch C et al. Plasma and brain matrix metalloproteinase-9 after acute focal cerebral ischemia in rats. Stroke 2009; 40 (8): 2836–42.
30. Asahi M, Asahi K, Jung JC et al. Role for matrix metalloproteinase 9 after focal cerebral ischemia: effects of gene knockout and enzyme inhibition with BB-94. J Cereb Blood Flow Metab 2000; 20: 1681–9.
31. Asahi M, Wang X, Mori T et al. Effects of matrix metalloproteinase-9 gene knockout on the proteolysis of blood-brain barrier and white matter components after cerebral ischemia. J Neurosci 2001; 21: 7724–32.
32. Gu Z, Kaul M, Yan B et al. S-nitrosylation of matrix metalloproteinases: Signaling pathway to neuronal cell death. Science 2002; 297: 1186–90.
33. Lee SR, Lo EH. Induction of caspase-mediated cell death by matrix metalloproteinases in cerebral endothelial cells after hypoxia-reoxygen-ation. J Cereb Blood Flow Metab 2004; 24: 720–7.
34. Copin JC, Merlani P, Sugawara Т et al. Delayed matrix metalloproteinase inhibition reduces intracerebral hemorrhage after embolic stroke in rats. Exp Neurol 2008; 213: 196–201.
35. Liu XS, Chopp M, Zhang RL. Angiopoietin 2 mediates the differentiation and migration of neural progenitor cells in the subventricular zone after stroke. J Biol Chem 2009; 284 (34): 22680–9.
36. Lee SR, Kim HY, Rogowska J et al. Involvement of matrix metalloproteinase in neuroblast cell migration from the subventricular zone after stroke. J Neurosci 2006; 26: 3491–5.
37. Rosenberg GA. Matrix metalloproteinases and their multiple roles in neurodegenerative diseases. Lancet Neurol 2009: 8: 205–16.
38. Montaner J, Alvarez-Sabin J, Molina CA et al. Matrix metalloproteinase expression is related to hemorrhagic transformation after cardioembolic stroke. Stroke 2001; 32: 2762–7.
39. Montaner J, Rovira A, Molina CA et al. Plasmatic level of neuroinflammatory markers predict the extent of diffusion-weighted image lesions in hyperacute stroke. J Cereb Blood Flow Metab 2003; 23: 1403–7.
40. Horstmann S, Kalb P, Koziol J et al. Profiles of matrix metalloproteinases, their inhibitors, and laminin in stroke patients: Influence of different therapies. Stroke 2003; 34: 2165–70.
41. Шамалов Н.А., Скворцова В.И., Рамазанов Г.Р. и др. Компьютерно-томографические и биохимические предикторы исходов тромболитической терапии у пациентов с ишемическим инсультом. Журн. неврологии и психиатрии им. С.С.Корсакова. 2010; 4: 21–8. / Shamalov N.A., Skvortsova V.I., Ramazanov G.R. i dr. Komp'iuterno-tomograficheskie i biokhimicheskie prediktory iskhodov tromboliticheskoi terapii u patsientov s ishemicheskim insul'tom. Zhurn. nevrologii i psikhiatrii im. S.S.Korsakova. 2010; 4: 21–8. [in Russian]
42. Coussens LM, Fingleton B, Matrisian LM. Matrix metalloproteinase inhibitors and cancer: trials and tribulations. Science 2002; 295: 2387–92.
43. Гусев Е.И., Коновалов А.Н., Скворцова В.И., Гехт А.Б. Неврология: Национальное руководство. М.: ГЭОТАР-Медиа, 2009; с. 592–615. / Gusev E.I., Konovalov A.N., Skvortsova V.I., Gekht A.B. Nevrologiia: Natsional'noe rukovodstvo. M.: GEOTAR-Media, 2009; s. 592–615. [in Russian]
44. Guidelines for management of ischaemic stroke and transient ischaemic attack 2008. Cerebrovasc Dis 2008; 25 (5): 457–507.
45. Suzuki Y. Role of tissue-type plasminogen activator in ischemic stroke. J Pharmacol Sci 2010; 113: 203–7.
46. Suzuki Y, Nagai N, Umemura K et al. Stromelysin-1 (MMP-3) is critical for intracranial bleeding after t-PA treatment of stroke in mice. J Thromb Haemost 2007; 5: 1732–9.
47. Hosomi N, Nishiyama A, Ban CR et al. Angiotensin type 1 receptor blockage improves ischemic injury following transient focal cerebral ischemia. Neuroscience 2005; 134: 225–31.
48. Tanaka H, Takai S, Jin D et al. Inhibition of matrix metalloproteinase-9 activity by trandolapril after middle cerebral artery occlusion in rats. Hypertens Res 2007; 5: 469–75.
49. Liebetrau M, Burggraf D, Wunderlich N et al. ACE inhibition reduces activity of the plas-minogen/plasmin and MMP systems in the brain of spontaneous hypertensive stroke-prone rats. Neurosci Lett 2005; 376: 205–9.
50. Miyazaki S, Kasai T, Miyauchi K et al. Changes of matrix metalloproteinase-9 level is associated with left ventricular remodeling following acute myocardial infarction among patients treated with trandolapril, valsartan or both. Circulation 2010; 74: 1158–64.
51. Hayashidani S, Tsutsui H, Shiomi T et al. Fluvastatin, a 3-hydroxyl-3-methylglutaryl coenzyme A reductase inhibitor, attenuates left ventricular remodelling and failure after experimental myocardial infarction. Circulation 2002; 105: 868–73.
52. Luan Z, Chase AJ, Newby AC. Statins inhibit secretion of metalloproteinases-1, -2, -3, and -9 from vascular smooth muscle cells and macrophages. Arterioscler Thromb Vas Biol 2003; 23: 769–75.
________________________________________________
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18. Welsh P, Whincup PH, Papacosta O. Serum matrix metalloproteinase-9 and coronary heart disease: a prospective study in middle-aged men. QJM 2008; 101: 785–91.
19. Kopitsa N.P., Belaia N.V., Titarenko N.V. Rol' matriksnykh metalloproteinaz v patogeneze postinfarktnogo remodelirovaniia levogo zheludochka. Mezhdunar. med. zhurn. 2010; 4: 55–58. [in Russian]
20. Cunningham LA, Wetzel M, Rosenberg GA. Multiple roles for MMPs and TIMPs in cerebral ischemia. Glia 2005; 50: 329–39.
21. Rosell A, Ortega-Aznar A. Alvarez-Sabin J et al. Increased brain expression of Matrix Metalloproteinase-9 after ischemic and hemorrhagic human stroke. Stroke 2006; 37: 1399–406.
22. Egashira Y, Zhao H, Hua Y et al. White Matter Injury After Subarachnoid Hemorrhage: Role of Blood-Brain Barrier Disruption and Matrix Metalloproteinase-9. Stroke 2015; 46 (10): 2909–5.
23. Cadenas I, Ribo M, Molina CA et al. Increased brain expression of matrix metalloproteinase-9 after ischemic and hemorrhagic human stroke. Stroke 2006; 37: 1399–406.
24. Zhao BQ, Ikeda Y, Ihara H et al. Essential role of endogenous tissue plasminogen activator through matrix metalloproteinase 9 induction and expression on heparin-produced cerebral hemorrhage after cerebral ischemia in mice. Blood 2004; 103: 2610–6.
25. Rosell A, Cuadrado E, Ortega-Aznar A. Mmp-9-positive neutrophil infiltration is associated to blood-brain barrier breakdown and basal lamina type iv collagen degradation during hemorrhagic transformation after human ischemic stroke. Stroke 2008; 39: 1121–6.
26. Romanic AM, White RF, Arleth AJ et al. Matrix metalloproteinase expression increases after cerebral focal ischemia in rats: Inhibition of matrix metalloproteinase-9 reduces infarct size. Stroke 1998; 5: 1020–30.
27. Planas AM, Sole S, Justicia C. Expression and activation of matrix metalloproteinase-2 and-9 in rat brain after transient focal cerebral ischemia. Neurobiol Dis 2001; 8: 834–46.
28. Koh SH, Chang DI, Kim HT et al. Effect of 3-aminobenzamide, parp inhibitor, on matrix metalloproteinase-9 level in plasma and brain of ischemic stroke model. Toxicology 2005; 214: 131–9.
29. Park KP, Rossel A, Foerch C et al. Plasma and brain matrix metalloproteinase-9 after acute focal cerebral ischemia in rats. Stroke 2009; 40 (8): 2836–42.
30. Asahi M, Asahi K, Jung JC et al. Role for matrix metalloproteinase 9 after focal cerebral ischemia: effects of gene knockout and enzyme inhibition with BB-94. J Cereb Blood Flow Metab 2000; 20: 1681–9.
31. Asahi M, Wang X, Mori T et al. Effects of matrix metalloproteinase-9 gene knockout on the proteolysis of blood-brain barrier and white matter components after cerebral ischemia. J Neurosci 2001; 21: 7724–32.
32. Gu Z, Kaul M, Yan B et al. S-nitrosylation of matrix metalloproteinases: Signaling pathway to neuronal cell death. Science 2002; 297: 1186–90.
33. Lee SR, Lo EH. Induction of caspase-mediated cell death by matrix metalloproteinases in cerebral endothelial cells after hypoxia-reoxygen-ation. J Cereb Blood Flow Metab 2004; 24: 720–7.
34. Copin JC, Merlani P, Sugawara Т et al. Delayed matrix metalloproteinase inhibition reduces intracerebral hemorrhage after embolic stroke in rats. Exp Neurol 2008; 213: 196–201.
35. Liu XS, Chopp M, Zhang RL. Angiopoietin 2 mediates the differentiation and migration of neural progenitor cells in the subventricular zone after stroke. J Biol Chem 2009; 284 (34): 22680–9.
36. Lee SR, Kim HY, Rogowska J et al. Involvement of matrix metalloproteinase in neuroblast cell migration from the subventricular zone after stroke. J Neurosci 2006; 26: 3491–5.
37. Rosenberg GA. Matrix metalloproteinases and their multiple roles in neurodegenerative diseases. Lancet Neurol 2009: 8: 205–16.
38. Montaner J, Alvarez-Sabin J, Molina CA et al. Matrix metalloproteinase expression is related to hemorrhagic transformation after cardioembolic stroke. Stroke 2001; 32: 2762–7.
39. Montaner J, Rovira A, Molina CA et al. Plasmatic level of neuroinflammatory markers predict the extent of diffusion-weighted image lesions in hyperacute stroke. J Cereb Blood Flow Metab 2003; 23: 1403–7.
40. Horstmann S, Kalb P, Koziol J et al. Profiles of matrix metalloproteinases, their inhibitors, and laminin in stroke patients: Influence of different therapies. Stroke 2003; 34: 2165–70.
41. Shamalov N.A., Skvortsova V.I., Ramazanov G.R. i dr. Komp'iuterno-tomograficheskie i biokhimicheskie prediktory iskhodov tromboliticheskoi terapii u patsientov s ishemicheskim insul'tom. Zhurn. nevrologii i psikhiatrii im. S.S.Korsakova. 2010; 4: 21–8. [in Russian]
42. Coussens LM, Fingleton B, Matrisian LM. Matrix metalloproteinase inhibitors and cancer: trials and tribulations. Science 2002; 295: 2387–92.
43. Gusev E.I., Konovalov A.N., Skvortsova V.I., Gekht A.B. Nevrologiia: Natsional'noe rukovodstvo. M.: GEOTAR-Media, 2009; s. 592–615. [in Russian]
44. Guidelines for management of ischaemic stroke and transient ischaemic attack 2008. Cerebrovasc Dis 2008; 25 (5): 457–507.
45. Suzuki Y. Role of tissue-type plasminogen activator in ischemic stroke. J Pharmacol Sci 2010; 113: 203–7.
46. Suzuki Y, Nagai N, Umemura K et al. Stromelysin-1 (MMP-3) is critical for intracranial bleeding after t-PA treatment of stroke in mice. J Thromb Haemost 2007; 5: 1732–9.
47. Hosomi N, Nishiyama A, Ban CR et al. Angiotensin type 1 receptor blockage improves ischemic injury following transient focal cerebral ischemia. Neuroscience 2005; 134: 225–31.
48. Tanaka H, Takai S, Jin D et al. Inhibition of matrix metalloproteinase-9 activity by trandolapril after middle cerebral artery occlusion in rats. Hypertens Res 2007; 5: 469–75.
49. Liebetrau M, Burggraf D, Wunderlich N et al. ACE inhibition reduces activity of the plas-minogen/plasmin and MMP systems in the brain of spontaneous hypertensive stroke-prone rats. Neurosci Lett 2005; 376: 205–9.
50. Miyazaki S, Kasai T, Miyauchi K et al. Changes of matrix metalloproteinase-9 level is associated with left ventricular remodeling following acute myocardial infarction among patients treated with trandolapril, valsartan or both. Circulation 2010; 74: 1158–64.
51. Hayashidani S, Tsutsui H, Shiomi T et al. Fluvastatin, a 3-hydroxyl-3-methylglutaryl coenzyme A reductase inhibitor, attenuates left ventricular remodelling and failure after experimental myocardial infarction. Circulation 2002; 105: 868–73.
52. Luan Z, Chase AJ, Newby AC. Statins inhibit secretion of metalloproteinases-1, -2, -3, and -9 from vascular smooth muscle cells and macrophages. Arterioscler Thromb Vas Biol 2003; 23: 769–75.
Авторы
Е.В.Константинова*, М.Х.Шурдумова
ГБОУ ВПО Российский национальный исследовательский медицинский университет им. Н.И.Пирогова Минздрава России. 117997, Россия, Москва, ул. Островитянова, д. 1
*katekons@mail.ru
ГБОУ ВПО Российский национальный исследовательский медицинский университет им. Н.И.Пирогова Минздрава России. 117997, Россия, Москва, ул. Островитянова, д. 1
*katekons@mail.ru
________________________________________________
E.V.Konstantinova*, M.Kh.Shurdumova
N.I.Pirogov Russian National Research Medical University of the Ministry of Health of the Russian Federation. 117997, Russian Federation, Moscow, ul. Ostrovitianova, d. 1
*katekons@mail.ru
N.I.Pirogov Russian National Research Medical University of the Ministry of Health of the Russian Federation. 117997, Russian Federation, Moscow, ul. Ostrovitianova, d. 1
*katekons@mail.ru
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