[Calcineurin contributed to tumor necrosis factor alpha-induced cardiomyocyte hypertrophy in rats].
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.


CONCLUSIONS
Ca(2+) -CaN signaling pathway are involved in cardiomyocyte hypertrophy induced by TNF-alpha in rats.
The First Affiliated Hospital, Liaoning Medical College, Jinzhou 121000, China. wgj-april@163.com
Gui-Jun
GJ
Wang
Yu-Sheng
YS
Yao
Hong-Xin
HX
Wang
Lian-Yi
LY
Guo
D000818:Animals; D019703:Calcineurin / Q000378:metabolism*; D020013:Calcium Signaling; D002311:Cardiomyopathy, Dilated / Q000378:metabolism* / Q000473:pathology; D002478:Cells, Cultured; D005260:Female; D008297:Male; D032383:Myocytes, Cardiac / Q000187:drug effects* / Q000378:metabolism* / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology*
D014409:Tumor Necrosis Factor-alpha; D019703:Calcineurin