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肥大刺激可诱导大鼠心室肌细胞中转化生长因子-β1的表达。

Hypertrophic stimuli induce transforming growth factor-beta 1 expression in rat ventricular myocytes.

作者信息

Takahashi N, Calderone A, Izzo N J, Mäki T M, Marsh J D, Colucci W S

机构信息

Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts 02115.

出版信息

J Clin Invest. 1994 Oct;94(4):1470-6. doi: 10.1172/JCI117485.

DOI:10.1172/JCI117485
PMID:7929822
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC295284/
Abstract

Transforming growth factor-beta 1 (TGF-beta 1) is a peptide growth factor that may play a role in the myocardial response to hypertrophic stimuli. However, the cellular distribution, mechanism of induction, and source of increased TGF-beta 1 in response to hypertrophic stimuli are not known. We tested the hypothesis that the cardiac myocyte responds to hypertrophic stimuli with the increased expression of TGF-beta 1. In adult rat ventricular myocardium freshly dissociated into myocyte and nonmyocyte cellular fractions, the preponderance of TGF-beta 1 mRNA visualized by Northern hybridization was in the nonmyocyte fraction. Abdominal aortic constriction (7 d) and subcutaneous norepinephrine infusion (36 h) each caused ventricular hypertrophy associated with 3.1-fold and 3.8-fold increases, respectively, in TGF-beta 1 mRNA in the myocyte fraction, but had no effect on the level of TGF-beta 1 mRNA in the nonmyocyte fraction. In ventricular myocytes, norepinephrine likewise caused a 4.1-fold increase in TGF-beta 1 mRNA associated with an increase in TGF-beta bioactivity. This induction of TGF-beta 1 mRNA occurred at norepinephrine concentrations as low as 1 nM and was blocked by prazosin, but not propranolol. NE did not increase the TGF-beta 1 mRNA level in nonmyocytes, primarily fibroblasts, cultured from neonatal rat ventricle. Thus, the cardiac myocyte responds to two hypertrophic stimuli, pressure overload and norepinephrine, with the induction of TGF-beta 1. These data support the view that TGF-beta 1, released by myocytes and acting in an autocrine and/or paracrine manner, is involved in myocardial remodeling by hypertrophic stimuli.

摘要

转化生长因子-β1（TGF-β1）是一种肽类生长因子，可能在心肌对肥厚刺激的反应中发挥作用。然而，TGF-β1在细胞中的分布、诱导机制以及对肥厚刺激反应时其表达增加的来源尚不清楚。我们检验了心肌细胞对肥厚刺激会通过增加TGF-β1表达做出反应这一假说。在刚分离成心肌细胞和非心肌细胞组分的成年大鼠心室心肌中，通过Northern杂交观察到的TGF-β1 mRNA主要存在于非心肌细胞组分中。腹主动脉缩窄（7天）和皮下注射去甲肾上腺素（36小时）均导致心室肥厚，同时心肌细胞组分中的TGF-β1 mRNA分别增加3.1倍和3.8倍，但对非心肌细胞组分中TGF-β1 mRNA的水平没有影响。在心室肌细胞中，去甲肾上腺素同样使TGF-β1 mRNA增加4.1倍，并伴有TGF-β生物活性的增加。TGF-β1 mRNA的这种诱导在去甲肾上腺素浓度低至1 nM时就会发生，且被哌唑嗪阻断，但不被普萘洛尔阻断。去甲肾上腺素并未增加从新生大鼠心室培养的非心肌细胞（主要是成纤维细胞）中TGF-β1 mRNA的水平。因此，心肌细胞对压力超负荷和去甲肾上腺素这两种肥厚刺激会通过诱导TGF-β1做出反应。这些数据支持这样一种观点，即由心肌细胞释放并以自分泌和/或旁分泌方式起作用的TGF-β1参与了肥厚刺激引起的心肌重塑。

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