MOLECULAR AND PHYSIOLOGOCAL MECHNISM OF VASCULAR INFLAMMATION AND REMODELING AFTER VASCULAR INJURY
MOLECULAR AND PHYSIOLOGOCAL MECHNISM OF VASCULAR INFLAMMATION AND REMODELING AFTER VASCULAR INJURY
批准号:
11670666
负责人:
IMAMURA Hiroshi
金额:
$2.43万
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (C)
财政年份:
1999
资助国家:
日本
项目状态:
已结题
起止时间:
1999 至 2000
中文摘要
A. P-选择素在血管损伤后炎症、新生内膜形成和血管重塑中的作用使用大鼠球囊导管诱导的损伤模型,我们检测了P-选择素在血管损伤过程中的作用。损伤后急性期,P-选择素在覆盖裸露节段的活化血小板和炎症外膜小血管的内皮细胞上均强烈表达。与对照组相比,连续8天用抗P-选择素单克隆抗体(MAb)治疗在第14天显著抑制新生内膜形成,并且这种作用持续到第56天。在第56天,伴随外膜纤维化的血管收缩也减弱。在第8天,CD 45阳性白细胞在新生内膜、中膜和外膜中的积累被抗P-选择素单克隆抗体治疗显著抑制。扫描电子显微镜显示,抗P-选择素治疗导致血栓形成的表面减少。 关于我们 动脉内膜,其特征是假内皮外观在损伤后14天。这些结果表明,抑制P-选择素介导的白细胞募集可防止新生内膜形成、外膜炎症和血管收缩的发展,并促进管腔平滑肌细胞的假内皮化。因此,这种处理有益地影响了大鼠球囊损伤后的血管重塑。B.球囊损伤后的动脉张力和对血管活性物质的反应为了评价血管损伤后血管张力和对增厚动脉壁的血管活性物质的反应,分离正常和球囊损伤的大鼠颈动脉,并测量周壁张力的变化。高钾治疗后球囊损伤动脉的基础血管张力降低。典型的血管收缩物质,去甲肾上腺素,苯肾上腺素,前列腺素(PG)F2-α,5羟色胺(5 HT)诱导的血管张力增加减弱,但相对反应相比,高钾诱导的收缩球囊损伤后没有改变。硝普钠引起的舒张作用减弱,但相对反应没有改变。少
英文摘要
A.Roles of P-Selectin in Inflammation, Neointimal Formation, and Vascular Remodeling after vascular injuryUsing a rat balloon catheter-induced injury model, we examined the role of P-selectin in vascular injury processes. In the acute phase after the injury, P-selectin was intensely expressed on both activated platelets covering the denuded segment and endothelial cells of the inflamed adventitial small vessels. Treatment with an anti-P-selectin monoclonal antibody (MAb) for 8 consecutive days significantly inhibited neointimal formation at day 14, and this effect persisted at day 56, as compared with the control group. Vascular shrinking accompanying adventitial fibrosis was also attenuated at day 56. Accumulation of CD45-positive leukocytes in the developing neointima, media and adventitia at day 8 was significantly inhibited by treatment with the anti-P-selectin MAb. Scanning electron microscopy demonstrated that anti-P-selectin treatment resulted in a less thrombogenic surface of t … More he arterial intima, which featured a pseudoendothelial appearance at day 14 after injury. These results suggest that inhibition of P-selectin-mediated leukocyte recruitment prevents the development of neointimal formation, adventitial inflammation, and vascular shrinking and promotes pseudoendothelialization by luminal smooth muscle cells. This treatment thus beneficially affects vascular remodeling after balloon injury in rat.B.Arterial Tone and Responses to Vasoactive Substances After Balloon InjuryTo evaluate vascular tone and response to vasoactive substances of thickening arterial wall after vascular injury, normal and balloon injured rat carotid arteries were isolated and change in circumferential wall tension was measured. Basic vascular tone of balloon injured artery after high potassium treatment was diminished. Typical vaso-constrictive substances, norepinephrine, phenylephrine, prostaglandin (PG) F2-alpha, and Serotonin (5HT) induced increases in vascular tension were attenuated, but relative responses compared with high potassium induced contraction were not changed after balloon injury. Relaxation induced by sodium nitroprusside was diminished, but relative responses were not changed. Less
期刊论文(3)
专著(0)
科研奖励(0)
会议论文
Hayashi S,Watanabe.N, et al: "Roles of P-selectin in Inflammation, Neointimal Formation, and Vascular Remodelingin Balloon Injured Rat Carotid Arteries."Circulation. 102. 1710-1717 (2000)
Hayashi S、Watanabe.N 等人:“P-选择素在球囊损伤大鼠颈动脉炎症、新内膜形成和血管重塑中的作用。”循环。
DOI:
--
发表时间:
期刊:
影响因子:
--
作者:
[]
通讯作者:
Kitabayashi H,Isobe M,Watanabe N, et al.: "FTY720 Prevents Development of Experimental Autoimmune Myocarditis through Reduction of Circulating Lymphocytes."Journal of Cardiovascular Pharmacology. 35. 410-416 (2000)
Kitabayashi H、Isobe M、Watanabe N 等人:“FTY720 通过减少循环淋巴细胞预防实验性自身免疫性心肌炎的发生。”心血管药理学杂志。
DOI:
--
发表时间:
期刊:
影响因子:
--
作者:
[]
通讯作者:
Imamura H,Momose T,Kitabayashi.H, et al: "Pulmonary hypertension as a result of asymptomatic portosystemic shunt."Japanese Circulation Journal. 64. 471-473 (2000)
Imamura H、Momose T、Kitabayashi.H 等人:“无症状门体分流导致的肺动脉高压。”日本循环杂志。
DOI:
--
发表时间:
期刊:
影响因子:
--
作者:
[]
通讯作者:
Alteration of delta-bilirubin concentration during biliary drainage and its relationships with plasma half-life of albumin and functional hepatocyte mass in patients with obstructive jaundice
-
批准号:20390352
-
项目类别:Grant-in-Aid for Scientific Research (B)
-
资助金额:$5.99万
-
财政年份:2008
-
负责人:IMAMURA Hiroshi
-
依托单位:
The effect of various methods of inflow occlusion techniques in a rat liver resection on the extent of the liver injury and liver regeneration
-
批准号:18591502
-
项目类别:Grant-in-Aid for Scientific Research (C)
-
资助金额:$2.51万
-
财政年份:2006
-
负责人:IMAMURA Hiroshi
-
依托单位:
Comprehensive analyses of liver regeneration-and atrophy-related genes in rat model of liver transplantation using size-mismatch graft
-
批准号:15591385
-
项目类别:Grant-in-Aid for Scientific Research (C)
-
资助金额:$2.18万
-
财政年份:2003
-
负责人:IMAMURA Hiroshi
-
依托单位:
Design of Electron-Spintronics devices
-
批准号:14076204
-
项目类别:Grant-in-Aid for Scientific Research on Priority Areas
-
资助金额:$12.42万
-
财政年份:2002
-
负责人:IMAMURA Hiroshi
-
依托单位:
Analysis of Wnt signaling pathway during cardiomyocyte differentiation
-
批准号:14570648
-
项目类别:Grant-in-Aid for Scientific Research (C)
-
资助金额:$2.18万
-
财政年份:2002
-
负责人:IMAMURA Hiroshi
-
依托单位:
Study of the liver tshemra/reperfusion injury recovery of the nepotocyte and sinnsoidol endotholial cell : invefvement of apoptosis and bile acrd depondent and indepondest ble flow.
-
批准号:13671219
-
项目类别:Grant-in-Aid for Scientific Research (C)
-
资助金额:$2.24万
-
财政年份:2001
-
负责人:IMAMURA Hiroshi
-
依托单位:
Involvement of MAC-1 (CD11b/CD18) and intercellular adhesion molecule (ICAM-1) in the ischemia reperfusion injury of rat liver in relation to sinusoidal endothelial cell damage and hepatocyte apoptosis
-
批准号:10671110
-
项目类别:Grant-in-Aid for Scientific Research (C)
-
资助金额:$2.37万
-
财政年份:1998
-
负责人:IMAMURA Hiroshi
-
依托单位:
海外基金