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Heat shock transcription factor 1 preserves cardiac angiogenesis and adaptation during pressure overload

Jiming Li¹, Junbo Ge¹, Jie Yuan¹, Hong Jiang¹, Hong Ma¹, Yanyan Liang¹, Yuhong Niu¹, Hui Gong¹, Ning Zhou¹, Aili Guan¹, Zhen Ma¹, Lingyan Yuan¹, Aijun Sun¹, Yuqi Wang², Akira Nakai³, Issei Komuro⁴ & Yunzeng Zou¹

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1. Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases
2. Zhongshan Hospital, Fudan University, Department of Vascular Surgery
3. Yamaguchi University School of Medicine,Department of Biochemistry and Molecular Biology
4. Chiba University Graduate School of Medicine, Department of Cardiovascular Science and Medicine

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Document Type:

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Date:

Received 24 December 2008 13:51 UTC; Posted 24 December 2008

Subjects:

Molecular Cell Biology

Tags:

• angiogenesis
• cardiovascular disease
• gene therapy
• miRNA

Abstract:

To examine how heat shock transcription factor 1 (HSF1) protects against maladaptive hypertrophy during pressure overload, we subjected HSF1 transgenic (TG), knockout (KO) and wild type (WT) mice to a constriction of transverse aorta (TAC), and found that cardiac hypertrophy, functions and angiogenesis were well preserved in TG mice but were decreased in KO mice compared to WT ones at 4 weeks, which was related to HIF-1 and p53 expression. Inhibition of angiogenesis suppressed cardiac adaptation in TG mice while overexpression of angiogenesis factors improved maladaptive hypertrophy in KO mice. In vitro formation of vasculatures by microvascular endothelial cells was higher in TG mice but lower in KO mice than in WT ones. A siRNA of p53 but not a HIF-1 gene significantly reversed maladaptive hypertrophy in KO mice whereas a siRNA of HIF-1 but not a p53 gene induced maladaptive hypertrophy in TG mice. Heart microRNA analysis showed that miR-378 and miR-379 were differently changed among the three mice after TAC, and miR-378 or siRNA of miR-379 could maintain cardiac adaptation in WT mice. These results indicate that HSF1 preserves cardiac adaptation during pressure overload through p53-HIF-1-associated angiogenesis, which is controlled by miR-378 and miR-379.

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This document is licensed to the public under the Creative Commons Attribution 3.0 License

How to cite this document:

Li, Jiming, Ge, Junbo, Yuan, Jie, Jiang, Hong, Ma, Hong, Liang, Yanyan, Niu, Yuhong, Gong, Hui, Zhou, Ning, Guan, Aili, Ma, Zhen, Yuan, Lingyan, Sun, Aijun, Wang, Yuqi, Nakai, Akira, Komuro, Issei, and Zou, Yunzeng. Heat shock transcription factor 1 preserves cardiac angiogenesis and adaptation during pressure overload. Available from Nature Precedings <http://hdl.handle.net/10101/npre.2008.2716.1> (2008)

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