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
de Zh
| WPRIM
| ID: wpr-340171
Bibliothèque responsable:
WPRO
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>
Texte intégral:
1
Indice:
WPRIM
Sujet Principal:
Anatomopathologie
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Pharmacologie
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Transduction du signal
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Morpholines
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Calcium
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4H-1-Benzopyran-4-ones
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Facteur de nécrose tumorale alpha
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Rat Sprague-Dawley
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Phosphatidylinositol 3-kinases
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Canaux calciques de type L
Limites du sujet:
Animals
langue:
Zh
Texte intégral:
Chinese Journal of Applied Physiology
Année:
2010
Type:
Article