Age-dependent changes in myocardial matrix metalloproteinase/tissue inhibitor of metalloproteinase profiles and fibroblast function
Age-dependent changes in myocardial matrix metalloproteinase/tissue inhibitor of metalloproteinase profiles and fibroblast function
复制标题
DOI：
10.1016/j.cardiores.2004.11.029
复制
发表时间：
2005-05-01
影响因子：
10.8
通讯作者：
Spinale, FG
中科院分区：
文献类型：
--
作者：
Lindsey, ML;Goshorn, DK;Spinale, FG
目的：为了评估左心室（LV）的几何形状，胶原蛋白水平，基质金属蛋白酶（NIMP）和金属蛋白酶组织抑制剂（TIMP）丰度，和心肌成纤维细胞function.Methods：年轻（3个月大; n=28），中年（MA; 15个月大; n=17），和老年（23个月大; n=16）CB 6 F1小鼠的性别在这项研究中使用的老化的影响。超声心动图参数进行了测量;胶原蛋白，MMP和TIMP水平测定的可溶性和不溶性蛋白组分;和成纤维细胞的功能进行了evaluated.Results：左心室舒张末期的尺寸和壁厚增加MA和老年小鼠，伴随着可溶性蛋白增加，不溶性胶原蛋白减少。免疫印迹显示差异MMP/TIMP的档案。与MA水平相比，老年小鼠不溶性部分中MMP-3、MMP-8、MMP-9、MMP-12和MMP-14增加，TIMP-3和TIMP-4减少，表明细胞外基质（ECM）降解能力增加。成纤维细胞的增殖是钝与age.Conclusion：这项研究，第一次，确定了具体的差异，可能有助于年龄依赖性ECM重塑的细胞和细胞外过程。(c)2004年欧洲心脏病学会。Elsevier B. V.出版，保留所有权利。
Objective: To evaluate the effects of aging on left ventricular (LV) geometry, collagen levels, matrix metalloproteinase (NIMP) and tissue inhibitor of metalloproteinase (TIMP) abundance, and myocardial fibroblast function.Methods: Young (3-month-old; n=28), middle-aged (MA; 15-month-old; n=17), and old (23-month-old; n=16) CB6F1 mice of both sexes were used in this study. Echocardiographic parameters were measured; collagen, MMP, and TIMP levels were determined for both the soluble and insoluble protein fractions; and fibroblast function was evaluated.Results: LV end-diastolic dimensions and wall thickness increased in both MA and old mice, accompanied by increased soluble protein and decreased insoluble collagen. Immunoblotting revealed differential MMP/TIMP profiles. Compared to MA levels, MMP-3, MMP-8, MMP-9, MMP-12, and MMP-14 increased, and TIMP-3 and TIMP-4 decreased in the insoluble fraction of old mice, suggesting increased extracellular matrix (ECM) degradative capacity. Fibroblast proliferation was blunted with age.Conclusion: This study, for the first time, identified specific differences in cellular and extracellular processes that likely contribute to age-dependent ECM remodeling. (c) 2004 European Society of Cardiology. Published by Elsevier B.V. All rights reserved.