Ca2+ is involved in tumor necrosis factor-alpha induced cardiomyocyte hypertrophy through PI3-kinase pathway in rats / 中国应用生理学杂志
Chinese Journal of Applied Physiology
;
(6): 284-288, 2010.
Article
in Chinese
| WPRIM
| ID: wpr-340171
ABSTRACT
<p><b>OBJECTIVE</b>To investigate whether Ca2+ contribute to cardiomyocyte hypertrophy induced by tumor necrosis factor-alpha (TNF-alpha) through PI3-kinase pathway.</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.</p><p><b>RESULTS</b>(1) TNF-alpha significantly induced the increase of protein content, [3H]-leucine incorporation and cell size. These responses were significantly suppressed by LY294002, a selective PI3-kinase inhibitor. Verapamil, L-type calcium channels antagonist, slightly attenuated TNF-alpha-induced these responses. (2) TNF-alpha increased the amplitude of the spontaneous Ca2+ transients in cultured ventricular myocytes from the neonatal rat; PI3-kinase inhibitor LY294002 could suppress the elevation induced by TNF-alpha, but calcium antagonist verapamil took the minor effects of TNF-alpha on [Ca2+]i metabolism.</p><p><b>CONCLUSION</b>Increasing the intercellular free Ca2+ level may play an essential role in TNF-alpha-induced cardiomyocyte hypertrophy through PI3-kinase pathway in rats, while L-type calcium channel takes the minor effects on it.</p>
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Pathology
/
Pharmacology
/
Signal Transduction
/
Morpholines
/
Calcium
/
Chromones
/
Tumor Necrosis Factor-alpha
/
Rats, Sprague-Dawley
/
Phosphatidylinositol 3-Kinases
/
Calcium Channels, L-Type
Limits:
Animals
Language:
Chinese
Journal:
Chinese Journal of Applied Physiology
Year:
2010
Type:
Article
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