The combined inhibition of the CaMKIIδ and calcineurin signaling cascade attenuates IGF?IIR?induced cardiac hypertrophy

ASIA unversity > 醫學暨健康學院 > 醫學檢驗暨生物技術學系 > 期刊論文 > Item 310904400/112707

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題名:	The combined inhibition of the CaMKIIδ and calcineurin signaling cascade attenuates IGF?IIR?induced cardiac hypertrophy
作者:	Ch, Chung?Hao;Chen, Chung?Hao;Lin, Jing?Wei;Lin, Jing?Wei;黃智洋;Huang, Chih?Yang;Yeh, Yu?Lan;Yeh, Yu?Lan;She, Chia?Yao;Shen, Chia?Yao;Farheen, Khan;Badrealam, Khan Farheen;Tsung?Jung, H;Ho, Tsung?Jung;Pa, V. Vijaya;Padma, V. Vijaya;Kuo, Wei?Wen;Kuo, Wei?Wen;黃志揚;Huang, Chih-Yang
貢獻者:	醫學檢驗暨生物技術學系
關鍵詞:	CaMKII;IGF-IIR;calcineurin;cardiac hypertrophy;hypertension.
日期:	2019-09
上傳時間:	2020-08-20 07:07:00 (UTC+0)
出版者:	亞洲大學
摘要:	Cardiac hypertrophy is a common phenomenon observed in progressive heart disease associated with heart failure. Insulin-like growth factor receptor II (IGF-IIR) has been much implicated in myocardial hypertrophy. Our previous studies have found that increased activities of signaling mediators, such as calcium/calmodulin-dependent protein kinase II (CaMKII) and calcineurin induces pathological hypertrophy. Given the critical roles played by CaMKII and calcineurin signaling in the progression of maladaptive hypertrophy, we anticipated that inhibition of CaMKII and calcineurin signaling may attenuate IGF-IIR-induced cardiac hypertrophy. The current study, therefore, investigated the effects of IGF-IIR activation on the CaMKII and calcineurin signaling and whether the combinatorial inhibition of the CaMKIIδ and calcineurin signaling could ameliorate IGF-IIR-induced pathological hypertrophy. In the present study, we induced IGF-IIR through the cardiomyocyte-specific transduction of IGFIIY27L via adeno-associated virus 2 (AAV2) to evaluate its effects on cardiac hypertrophy. Interestingly, it was observed that the activation of IGF-IIR signaling through IGFIIY27L induces significant hypertrophy of the myocardium and increased cardiac apoptosis and fibrosis. Moreover, we found that Leu27 IGF-II significantly induced calcineurin and CaMKII expression. Furthermore and importantly, the combinatorial treatment with CaMKII and calcineurin inhibitors significantly alleviates IGF-IIR-induced hypertrophic responses. Thus, it could be envisaged that the inhibition of IGF-IIR may serve as a promising candidate for attenuating maladaptive hypertrophy. Both calcineurin and CaMKII could be valuable targets for developing treatment strategies against hypertension-induced cardiomyopathies.
關聯:	JOURNAL OF CELLULAR PHYSIOLOGY
顯示於類別:	[醫學檢驗暨生物技術學系] 期刊論文

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