The Role of Calcium Affecting Signal Pathway Related to Nitric Oxide-induced Cytotoxicity in H9c2 Cardiac Myoblast / 대한해부학회지
Korean Journal of Anatomy
;
: 587-594, 2000.
Article
in Korean
| WPRIM
| ID: wpr-651161
ABSTRACT
Nitric oxide (NO) elevates intracellular calcium. But the actions of calcium in NO-induced cell death are not well understood. This study was carried out to investigate the signal transduction pathways of calcium and NO-induced cytotoxicity in H9c2 cardiac myoblasts by using NO donor compounds such as sodium nitroprusside (SNP) and S-nitroso-N-acetylpenicillamine (SNAP). Pretreatment of intracellular calcium chelating agent (BAPTA/AM) or L-type calcium channel blockers (nicardipine, nifedipine, diltiazem and veraparmil) or T-type calcium channel blocker (flunarizine) blocked SNP-induced cytotoxicity respectively only in a three hours. However, thapsigargin (TG), which inhibits endoplasmic reticulum dependent Ca(2+)-ATPase and thereby increases cytosolic Ca(2+), augmented SNP-induced cytotoxicity. The protective effect of BAPTA/AM was inhibited by treatment of protein synthesis inhibitor, cyclohexamide. In addition, pyrrolidine dithiocarbamate (PDTC), NF-kB inhibitor, attenuates the protective effect of BAPTA/AM against SNP-induced cytotoxicity. It is indicated that the protective effect of BAPTA/AM against NO-induced cytotoxicity might be due to the expression of protein related to activation of NFkB. From these results, it is concluded that SNP-induced cytotoxicity is mediated by calcium in a 3 hours via down regulation of protein expression rleated to activation of NFkB.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Tissue Donors
/
Nitroprusside
/
Diltiazem
/
Nifedipine
/
Signal Transduction
/
Down-Regulation
/
Calcium
/
NF-kappa B
/
Cell Death
/
Thapsigargin
Limits:
Humans
Language:
Korean
Journal:
Korean Journal of Anatomy
Year:
2000
Type:
Article
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