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Chinese Journal of Applied Physiology ; (6): 184-188, 2012.
Article in Chinese | WPRIM | ID: wpr-329914

ABSTRACT

<p><b>OBJECTIVE</b>To investigate whether calcineurin (CaN) contribute to tumor necrosis factor alpha (TNF-alpha)-induced cardiomyocyte hypertrophy.</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>(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.</p><p><b>CONCLUSION</b>Ca(2+) -CaN signaling pathway are involved in cardiomyocyte hypertrophy induced by TNF-alpha in rats.</p>


Subject(s)
Animals , Female , Male , Rats , Calcineurin , Metabolism , Calcium Signaling , Cardiomyopathy, Dilated , Metabolism , Pathology , Cells, Cultured , Myocytes, Cardiac , Metabolism , Pathology , Rats, Sprague-Dawley , Tumor Necrosis Factor-alpha , Pharmacology
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