Thyroid hormone induces myocardial matrix degradation by activating matrix metalloproteinase-1
Thyroid hormone induces myocardial matrix degradation by activating matrix metalloproteinase-1
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DOI：
10.1016/j.matbio.2006.12.005
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发表时间：
2007-05-01
期刊：
影响因子：
6.9
通讯作者：
Bandyopadhyay, Arun
中科院分区：
文献类型：
--
作者：
Roy, Sreerupa Ghose;Mishra, Sumita;Bandyopadhyay, Arun
甲状腺功能亢进患者发生左心室肥大，与几个心脏参数（如心率、心输出量、心脏收缩和血流动力学超负荷）的改变相关，导致心脏并发症。甲状腺功能亢进时，虽然会发生心肌肥大和收缩异常，但通常不会发生心肌间质纤维化。因此，在本研究中，调节甲状腺功能亢进状态下心肌细胞外基质（ECM）重塑的机制进行了研究。通过给予3，5，3 '-三碘-L-甲状腺原氨酸（三碘甲状腺原氨酸，8 μ g/100 g BW，ip，SID）和糖皮质激素地塞米松（DEX，35 μ g/100 g BW，po，SID）（也是肥大诱导剂）15天，在Sprague-Dawley大鼠中产生心脏肥大。与对照组相比，三碘甲状腺原氨酸和DEX治疗组大鼠的心脏/体重比以及心房和脑利钠肽mRNA均显著增加。胶原蛋白-I和-III沉积在左心室部分减少三碘甲状腺原氨酸治疗的大鼠，而在DEX治疗的动物相比，这些增加。而三碘甲状腺原氨酸可使前胶原-I和-III的mRNA和蛋白水平升高（p
Hyperthyroid patients develop left ventricular hypertrophy associated with alterations of several cardiac parameters such as heart rate, cardiac output, cardiac contraction and hemodynamic overload leading to cardiac complications. Although cardiac hypertrophy and contractile abnormality occur, interstitial fibrosis in the heart usually does not take place in hyperthyroid condition. Therefore, in the present study, the mechanism regulating myocardial extracellular matrix (ECM) remodeling in hyperthyroid condition was investigated. Cardiac hypertrophy was developed in Sprague-Dawley rats by administration of 3,5,3'-triiodo-L-thyronine (triiodothyronine, 8 mu g/100g BW, ip, SID) and glucocorticosteroid, dexamethasone (DEX, 35 mu g/100g BW, po, SID), which is also an inducer of hypertrophy for 15 days. Heart/Body weight ratio and atrial and brain natriuretic peptide mRNAs were significantly increased in both triiodothyronine- and DEX-treated rats compared to control. Collagens-I and -III deposition in the left ventricular sections was reduced in triiodothyronine-treated rats, whereas in DEX-treated animals those were increased compared to control. While mRNA and protein levels of procollagens-I and -III were increased with triiodothyronine (p