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Updated: May 21, 2026

Transverse Aortic Constriction in Mice
Published on: April 21, 2010
[Calcineurin contributed to tumor necrosis factor alpha-induced cardiomyocyte hypertrophy in rats]
Gui-Jun Wang1, Yu-Sheng Yao, Hong-Xin Wang
1The First Affiliated Hospital, Liaoning Medical College, Jinzhou 121000, China. wgj-april@163.com
Objective:
To investigate whether calcineurin (CaN) contribute to tumor necrosis factor alpha (TNF-alpha)-induced cardiomyocyte hypertrophy.
Methods:
The protein content was assayed with lowry's method. The cardiomyocytes volumes were measured by computer photograph analysis system. The protein synthesis was assayed with [3H]-leucine incorporation method. [Ca2+]i transient was measured by Till image system by cell-loading Fura-2/AM. The expression of CaN was determined by Western blot.
Results:
(1) (CsA (0.2 micromol/L), a selective CaN inhibitor, significantly suppressed the increase of protein content, [3H]-leucine incorporation and cell size induced by TNF-alpha. (2) CsA (0.2 micromol/L) significantly suppressed the elevation of the amplitude of the spontaneous Ca2+ transients induced by TNF-alpha in cultured ventricular myocytes from the neonatal rat. (3) TNF-alpha significantly increased the expression of CaN.
Conclusion:
Ca(2+) -CaN signaling pathway are involved in cardiomyocyte hypertrophy induced by TNF-alpha in rats.
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