PRESSURE-INDUCED AND VOLUME-INDUCED LEFT-VENTRICULAR HYPERTROPHIES ARE ASSOCIATED WITH DISTINCT MYOCYTE PHENOTYPES AND DIFFERENTIAL INDUCTION OF PEPTIDE GROWTH-FACTOR MESSENGER-RNAS
PRESSURE-INDUCED AND VOLUME-INDUCED LEFT-VENTRICULAR HYPERTROPHIES ARE ASSOCIATED WITH DISTINCT MYOCYTE PHENOTYPES AND DIFFERENTIAL INDUCTION OF PEPTIDE GROWTH-FACTOR MESSENGER-RNAS
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DOI：
10.1161/01.cir.92.9.2385
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发表时间：
1995-11-01
期刊：
影响因子：
37.8
通讯作者：
COLUCCI, WS
中科院分区：
文献类型：
--
作者：
CALDERONE, A;TAKAHASHI, N;COLUCCI, WS
慢性压力和容量过载（PO和VO）导致心肌肥大在形态和功能上的不同形式。我们验证了PO和vo诱导的左心室肥大与肽生长因子诱导的不同分子表型和模式相关的假设。方法和结果分别对肾上主动脉收缩引起的左室肥厚大鼠左室心肌mRNA水平进行定量分析，左室肥厚大鼠左室心肌mRNA水平为1周。虽然PO和VO引起左室重量和房前利钠因子mRNA的相当增加，但PO而不是VO增加了胎儿基因-肌球蛋白重链和骨骼α -肌动蛋白的mRNA水平，并降低了肌浆网Ca2+ atp酶的mRNA水平。在心肌细胞富集的心肌片段中，转化生长因子- β(3)和胰岛素样生长因子-1 mRNA水平随PO升高而不随VO升高；酸性成纤维细胞生长因子mRNA在PO组无明显变化，而VO组明显降低。在非肌细胞富集的心肌片段中，VO降低了转化生长因子-p和胰岛素样生长因子-1 mRNA水平，但PO不变。结论PO-和vo -诱导的左室肥大与肽生长因子诱导的不同分子表型和模式相关。信号事件和肽生长因子与基因表达耦合的刺激特异性异质性可能在决定由各种形式的血流动力学过载引起的肥厚类型中发挥作用。
Background Chronic pressure and volume ocerload (PO and VO) result in morphologically and functionally distinct forms of myocardial hypertrophy. We tested the hypothesis that PO- and VO-induced left ventricular (LV) hypertrophies are associated with distinct molecular phenotypes and patterns of peptide growth factor induction.Methods and Results mRNA levels were quantified in LV myocardium from rats with LV hypertrophy due to PO or VO caused by suprarenal aortic constriction or an abdominal aortocaval fistula, respectively, for 1 week. Although PO and VO caused comparable increases in LV weight and preproatrial natriuretic factor mRNA, PO but not VO increased mRNA levels for the fetal genes beta-myosin heavy chain and skeletal alpha-actin and reduced the mRNA level of sarcoplasmic reticulum Ca2+ ATPase. In a myocyte-enriched myocardial fraction, transforming growth factor-beta(3) and insulin-like growth factor-1 mRNA levels were increased with PO but not VO; acidic fibroblast growth factor mRNA was unchanged with PO but decreased with VO. In a nonmyocyte-enriched myocardial fraction, transforming growth factor-p, and insulin-like growth factor-1 mRNA levers were decreased with VO but unchanged with PO.Conclusions PO- and VO-induced LV hypertrophies are associated with distinct molecular phenotypes and patterns of peptide growth factor induction. Stimulus-specific heterogeneity in the signaling events and peptide growth factors coupled to gene expression could play a role in determining the type of hypertrophy that is caused by various forms of hemodynamic overload.