Role of Polymorphic Variants of Gene of Inducible NO Synthase NOS2 in Brain Infarction in Patients with Acute Ischemic Stroke

被引:6
作者
Tupitsyna, T. V. [1 ]
Bondarenko, E. A. [1 ]
Botsina, A. Yu. [2 ]
Shetova, I. M. [2 ]
Limborskaya, S. A. [1 ]
Skvortsova, V. I. [2 ]
Slominskii, P. A. [1 ]
机构
[1] Russian Acad Sci, Inst Mol Genet, Moscow, Russia
[2] Russian State Med Univ, Moscow 117437, Russia
关键词
gene polymorphism; ischemic stroke; inducible NO synthase; brain infarction; dynamics of ischemic focus volume; NITRIC-OXIDE SYNTHASE; CEREBRAL-ISCHEMIA; MICE LACKING; EXPRESSION; REDUCTION; INJURY;
D O I
10.3103/S0891416810030018
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
Cerebrovascular diseases, including stroke, are an important problem in public health. Stroke development depends on external factors and the individual genetic specificity of the patient. Excessive NO production by inducible NO synthase (iNOS) damages brain tissue at various stages of the disease. The goal of this work was to study the role of four polymorphic variants of gene of inducible NO synthase iNOS (-2447C/G,. -1659C/T, -0.7(TTTA)n I/D, S608L (150C/T)) in brain infarction in patients with acute ischemic stroke. A statistically significant correlation between S608L (150C/T) polymorphism and infarction dynamics was observed during days 1-3 and 7-21 after infarction. These parameters correlate to the neurological status, which is estimated using the Orgogozo scale during days 1-7 of disease development. It was demonstrated that the C150C genotype was associated with ischemic focus propagation, regardless of its volume and neurological status by Orgogozo scale in patients with acute stroke. In the case of low initial volume, it was observed that the C150C genotype had an effect on ischemic damage during days 1-3.
引用
收藏
页码:89 / 94
页数:6
相关论文
共 21 条
[1]
Endothelial cell activation by endotoxin involves superoxide/NO-mediated nitration of prostacyclin synthase and thromboxane receptor stimulation [J].
Bachschmid, M ;
Thurau, S ;
Zou, MH ;
Ullrich, V .
FASEB JOURNAL, 2003, 17 (03) :914-+
[2]
Beck KF, 1999, J EXP BIOL, V202, P645
[3]
Inducible nitric oxide synthase appears and is co-expressed with the neuronal isoform in interneurons of the rat hippocampus after transient ischemia induced by middle cerebral artery occlusion [J].
Corsani, Letizia ;
Bizzoco, Elisa ;
Pedata, Felicita ;
Gianfriddo, Marco ;
Faussone-Pellegrini, Maria Simonetta ;
Vannucchi, Maria Giuliana .
EXPERIMENTAL NEUROLOGY, 2008, 211 (02) :433-440
[4]
Pathobiology of ischaemic stroke: an integrated view [J].
Dirnagl, U ;
Iadecola, C ;
Moskowitz, MA .
TRENDS IN NEUROSCIENCES, 1999, 22 (09) :391-397
[5]
The physiology and pathophysiology of nitric oxide in the brain [J].
Guix, FX ;
Uribesalgo, I ;
Coma, M ;
Muñoz, FJ .
PROGRESS IN NEUROBIOLOGY, 2005, 76 (02) :126-152
[6]
Gusev E.I., 2001, ISHEMIYA GOLOVNOGO M
[7]
Molecular pathology of cerebral ischemia: Delayed gene expression and strategies for neuroprotection [J].
Iadecola, C ;
Ross, ME .
FRONTIERS OF NEUROLOGY: A SYMPOSIUM IN HONOR OF FRED PLUM, 1997, 835 :203-217
[8]
INDUCIBLE NITRIC-OXIDE SYNTHASE GENE-EXPRESSION IN BRAIN FOLLOWING CEREBRAL-ISCHEMIA [J].
IADECOLA, C ;
ZHANG, FG ;
XU, S ;
CASEY, R ;
ROSS, ME .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1995, 15 (03) :378-384
[9]
Iadecola C, 1997, J NEUROSCI, V17, P9157
[10]
Illarioshkin S.N., 2005, OCHERKI ANGIONEVROLO