Hyperglycemia-induced TGFbeta and fibronectin expression in embryonic mouse heart.
Hyperglycemia-induced TGFbeta and fibronectin expression in embryonic mouse heart.
复制标题
高血糖诱导胚胎小鼠心脏中 TGFbeta 和纤连蛋白的表达。
DOI：
10.1002/dvdy.20123
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发表时间：
2004
期刊：
影响因子：
--
通讯作者：
Smoak,IdaWashington
中科院分区：
文献类型：
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作者：
Smoak,IdaWashington
心血管缺陷在糖尿病后代中很常见，但对其病因和发病机制知之甚少。细胞外基质因高血糖而在成人组织中积聚，转化生长因子-β1 (TGFβ1) 可能介导这种效应。本研究的目的是表征器官发生阶段小鼠心脏中 TGFβ 的表达，并评估暴露于高血糖的胚胎小鼠心脏中 TGFβ 和纤连蛋白的表达。在胚胎日 (E) 9.5–E13.5 心脏中证实了显着的 TGFβ1 和最少的 TGFβ2 或 TGFβ3 蛋白表达。免疫组织化学显示，24 小时高血糖导致纤连蛋白显着增加，TGFβ1 略有增加，TGFβ2 或 TGFβ3 未变化。通过酶联免疫吸附测定，在高血糖 24 小时（而非 48 小时）后胚胎液和离体心脏中发现 TGFβ1 增加。 24小时后高血糖增加了胚胎心脏中纤连蛋白和mRNA的表达，心包注射TGFβ1也增加了胚胎心脏中纤连蛋白mRNA的表达。有人提出，TGFβ1 和纤连蛋白可能在糖尿病引起的心脏畸形发生中发挥作用。发展动力学 231:179–189, 2004。© 2004 Wiley-Liss, Inc.
Cardiovascular defects are common in diabetic offspring, but their etiology and pathogenesis are poorly understood. Extracellular matrix accumulates in adult tissues in response to hyperglycemia, and transforming growth factor‐beta1 (TGFβ1) likely mediates this effect. The objective of this study was to characterize TGFβ expression in the organogenesis‐stage mouse heart and to evaluate TGFβ and fibronectin expression in embryonic mouse heart exposed to hyperglycemia. Prominent TGFβ1, and minimal TGFβ2 or TGFβ3, protein expression was demonstrated in embryonic day (E) 9.5–E13.5 hearts. Hyperglycemia for 24 hr produced significantly increased fibronectin, slightly increased TGFβ1, and unchanged TGFβ2 or TGFβ3, by immunohistochemistry. Increased TGFβ1 was demonstrated by enzyme‐linked immunosorbent assay in embryonic fluid and isolated hearts after hyperglycemia for 24 hr, but not 48 hr. Hyperglycemia increased fibronectin protein and mRNA expression in embryonic hearts after 24 hr, and pericardial injection of TGFβ1 also increased fibronectin mRNA in the embryonic heart. It is proposed that TGFβ1 and fibronectin may play a role in diabetes‐induced cardiac dysmorphogenesis. Developmental Dynamics 231:179–189, 2004. © 2004 Wiley‐Liss, Inc.