Shintani-Ishida Kaori, Unuma Kana, Yoshida Ken-ichi
Department of Forensic Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Circ J. 2009 Sep;73(9):1661-8. doi: 10.1253/circj.cj-09-0079. Epub 2009 Jul 9.
In ischemia-reperfusion, contraction band necrosis (CBN) is distributed mainly to the lateral border of the risk area and does not spread into the non-risk area beyond the border. It has been suggested that CBN is propagated through gap junctions (GJs), but it is unclear how GJs transmit CBN exclusively in the risk area.
Coronary occlusion for 30 min in rat increased the level of connexin43 (Cx43) protein in the 100,000 x g pellet fraction to 1.5-fold and decreased that in the 1,000 x g pellet to half in the risk area compared with the non-risk area. Immunohistochemical analysis showed an increase of Cx43 at intercalated disks in the risk area. A dye transfer assay demonstrated enhancement of GJ intercellular communication (GJIC) in the risk area compared with the non-risk area in the same section. Administration of a GJ blocker, carbenoxolone, at the onset of reperfusion following 30 min of ischemia reduced the CBN area (1/3 vs PBS) in 5 min of reperfusion and limited the infarct size (2/3 vs PBS) in 6 h of reperfusion.
These data suggest that ischemia enhances translocation of Cx43 to GJs, thereby promoting propagation of CBN exclusively in the risk area through enhanced GJIC after reperfusion.
在缺血再灌注过程中，收缩带坏死（CBN）主要分布在危险区域的外侧边界，不会扩散到边界以外的非危险区域。有人提出CBN是通过缝隙连接（GJ）传播的，但尚不清楚GJ如何仅在危险区域传播CBN。
与非危险区域相比，大鼠冠状动脉闭塞30分钟后，危险区域中100,000 x g沉淀组分中的连接蛋白43（Cx43）蛋白水平增加至1.5倍，而1,000 x g沉淀中的水平降低至一半。免疫组织化学分析显示危险区域闰盘中Cx43增加。染料转移试验表明，与同一切片中的非危险区域相比，危险区域中的GJ细胞间通讯（GJIC）增强。在缺血30分钟后的再灌注开始时给予GJ阻滞剂甘草次酸，可在再灌注5分钟时减少CBN面积（与PBS相比为1/3），并在再灌注6小时时限制梗死面积（与PBS相比为2/3）。
这些数据表明，缺血增强了Cx43向GJ的转位，从而在再灌注后通过增强的GJIC促进CBN仅在危险区域传播。
