Cerebral ischemia and angiogenesis

被引:83
作者
Hayashi, Takeshi [1 ]
Deguchi, Kentaro [1 ]
Nagotani, Shoko [1 ]
Zhang, Hanzhe [1 ]
Sehara, Yoshihide [1 ]
Tsuchiya, Atsushi [1 ]
Abe, Koji [1 ]
机构
[1] Okayama Univ, Grad Sch Med & Dent, Dept Neurol, Okayama 7008558, Japan
关键词
brain edema; endothelial cell; extracellular matrix; growth factor; neuroprotection; pericyte; therapeutics; vessel;
D O I
10.2174/156720206776875902
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Angiogenesis occurs in a wide range of conditions. As ischemic tissue usually depends on collateral blood flow from newly produced vessels, acceleration of angiogenesis should be of therapeutic value to ischernic disorders. Indeed, therapeutic angiogenesis reduced tissue injury in myocardial or limb ischemia. In ischernic stroke, on the other hand, angiogenic factors often increase vascular permeability and thus may deteriorate tissue damage. In order to apply safely the therapeutic angiogenesis for ischemic stroke treatment, elucidating precise mechanism of brain angiogenesis is mandatory, In the present article, we review previous reports which investigated molecular mechanisms of angiogenesis. Endothelial cell mitogens, enzymes that degrade surrounding extracellular matrix, and molecules implicated in endothelial cells migration are induced rapidly in the ischernic brain. Their possible neuroprotective or injury exacerbating effects are discussed. Because therapeutic potential of angiogenic factors application had gained much attention, we here extensively reviewed relevant previous reports. In the future however, there is a need to consider angiogenesis in relation with regenerative medicine, as angiogenic factors sometimes possess neuron producing property.
引用
收藏
页码:119 / 129
页数:11
相关论文
共 117 条
[1]   Activated microvessels express vascular endothelial growth factor and integrin αVβ3 during focal cerebral ischemia [J].
Abumiya, T ;
Lucero, J ;
Heo, JH ;
Tagaya, M ;
Koziol, JA ;
Copeland, BR ;
del Zoppo, GJ .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1999, 19 (09) :1038-1050
[2]   PREDICTING THE OUTCOME OF ACUTE STROKE - A PROGNOSTIC SCORE [J].
ALLEN, CMC .
JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY, 1984, 47 (05) :475-480
[3]   Endothelial/pericyte interactions [J].
Armulik, A ;
Abramsson, A ;
Betsholtz, C .
CIRCULATION RESEARCH, 2005, 97 (06) :512-523
[4]   Tie2 receptor ligands, angiopoietin-1 and angiopoietin-2, modulate VEGF-induced postnatal neovascularization [J].
Asahara, T ;
Chen, DH ;
Takahashi, T ;
Fujikawa, K ;
Kearney, M ;
Magner, M ;
Yancopoulos, GD ;
Isner, JM .
CIRCULATION RESEARCH, 1998, 83 (03) :233-240
[5]   Role for matrix metalloproteinase 9 after focal cerebral ischemia, effects of gene knockout and enzyme inhibition with BB-94 [J].
Asahi, M ;
Asahi, K ;
Jung, JC ;
del Zoppo, GJ ;
Fini, ME ;
Lo, EH .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 2000, 20 (12) :1681-1689
[6]   INVIVO PATTERNS OF EXPRESSION OF UROKINASE AND ITS INHIBITOR PAI-1 SUGGEST A CONCERTED ROLE IN REGULATING PHYSIOLOGICAL ANGIOGENESIS [J].
BACHARACH, E ;
ITIN, A ;
KESHET, E .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1992, 89 (22) :10686-10690
[7]   Extensive vasculogenesis, angiogenesis, and organogenesis precede lethality in mice lacking all αv integrins [J].
Bader, BL ;
Rayburn, H ;
Crowley, D ;
Hynes, RO .
CELL, 1998, 95 (04) :507-519
[8]   ANGIOGENIC-INDUCED ENHANCEMENT OF COLLATERAL BLOOD-FLOW TO ISCHEMIC MYOCARDIUM BY VASCULAR ENDOTHELIAL GROWTH-FACTOR IN DOGS [J].
BANAI, S ;
JAKLITSCH, MT ;
SHOU, M ;
LAZAROUS, DF ;
SCHEINOWITZ, M ;
BIRO, S ;
EPSTEIN, SE ;
UNGER, EF .
CIRCULATION, 1994, 89 (05) :2183-2189
[9]   Autologous mesenchymal stem cell transplantation in stroke patients [J].
Bang, OY ;
Lee, JS ;
Lee, PH ;
Lee, G .
ANNALS OF NEUROLOGY, 2005, 57 (06) :874-882
[10]   Expression of angiopoietin-1, angiopoietin-2, and tie receptors after middle cerebral artery occlusion in the rat [J].
Beck, H ;
Acker, T ;
Wiessner, C ;
Allegrini, PR ;
Plate, KH .
AMERICAN JOURNAL OF PATHOLOGY, 2000, 157 (05) :1473-1483