Activation of matrix metalloproteinase dilates and decreases cardiac tensile strength
Activation of matrix metalloproteinase dilates and decreases cardiac tensile strength
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DOI：
10.1016/s0167-5273(01)00449-1
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发表时间：
2001-07-01
影响因子：
3.5
通讯作者：
Tyagi, SC
中科院分区：
文献类型：
--
作者：
Mujumdar, VS;Smiley, LM;Tyagi, SC
先前的研究表明，自发性高血压大鼠（SHR）从代偿性压力超负荷肥大到失代偿性容量超负荷心力衰竭的转变与心脏抗拉强度降低和基质金属蛋白酶（MMP）激活相关。为了检验这一假设，即心力衰竭期间 MMP 缺乏一氧化氮激活会导致细胞外基质 (ECM) 组织破坏并导致收缩期和舒张期心脏拉伸强度降低，我们采用了 24-32 周的 SHR，这表明存在显着的心脏肥厚和纤维化。正常血压 Wistar 大鼠（NWR）用作对照。确定心脏肥大是否与弹性蛋白基质金属蛋白酶-2 (MMP-2) 活性增加有关；对心脏组织匀浆进行定量弹性蛋白酶谱分析。 MMP-2 活性通过肌动蛋白水平标准化。 SHR32wks 的左心室 (LV) 中 MMP-2/肌动蛋白比率为 2.0 +/-0.5，右心室 (RV) 为 1.5 +/-0.25，NWR32wks 的 LV 为 0.5 +/-0.25，RV 为 0.25 +/-0.12，(P
Previous studies demonstrated that transition from compensatory pressure overload hypertrophy to decompensatory volume overload heart failure is associated with decreased cardiac tensile strength and activation of matrix metalloproteinase (MMP) in spontaneously hypertensive rat (SHR). To test the hypothesis that in the absence of nitric oxide activation of MMP during cardiac failure causes disruption in the organization of extracellular matrix (ECM) and leads to decrease systolic and diastolic cardiac tensile strength, we employed SHR of 24-32 weeks, which demonstrates significant cardiac hypertrophy and fibrosis. The normotensive Wistar rats (NWR) were used as control. To determine whether cardiac hypertrophy is associated with increased elastinolytic matrix metalloproteinase-2 (MMP-2) activity; quantitative elastin-zymography was performed on cardiac tissue homogenates. The MMP-2 activity was normalized by the levels of actin. The MMP-2/actin ratio was 2.0 +/-0.5 in left ventricle (LV) and 1.5 +/-0.25 in right ventricle (RV) of SHR32wks and 0.5 +/-0.25 in LV and 0.25 +/-0.12 in RV of NWR32wks, (P