Sodium Nitroprusside로 유발한 HaCaT Cell의 Apoptosis
Induction of HaCaT Cell Apoptosis by Sodium Nitroprusside
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초록
산화질소(Nitric Oxide, NO)는 생리학적, 병리학적으로 주요한 역할을 하고 있는 것으로 알려져 있다. 본 실험에서는 NO donor인 sodium nitroprusside (SNP)가 HaCaT 세포에서 apoptosis를 유도한다는 것을 DAPI염색과 PARP, caspase-3 단백질 절단을 western blot으로 확인하였다. SNP는 ER stress와 관련 있는 Bip, CHOP 유전자 발현에는 영향이 없었다. 최근 NAD+ 의존 deacetylase인 sirt1이 세포의 생존 및 사멸에 매우 중요한 단백질이라는 보고가 있다. 본 실험에서 SNP는 HaCaT 세포의 sirt1 유전자 발현을 감소시켰으며 이는 apoptosis와 관련이 있을 수 있다.
Abstract
Nitric Oxide (NO) has been known to play important physiological and pathological roles. In this study, Sodium nitroprusside (SNP), NO donor, induced the apoptosis of HaCaT cell, human spontaneous immortal keratinocyte, which was investigated through DAPI staining and cleavage of PARP and caspase-3 protein. However, the expression level of Bip and CHOP, involved in ER stress, was not significantly changed as compared to the control cell group. Recent studies have showed that SIRT1, NAD+-dependent deacetylase, is the key protein that controls cell survival and death. SNP treatment suppressed the SIRT1 gene expression, which indicated that apoptosis induced by SNP could be implicated in SIRT1 down-regulation.
참고문헌 (17)
- Bastianetto S, "Protective Action of Resveratrol in Human Skin:Possible Involvement of Specific Receptor Binding Sites", PLos ONE, 5(9), pp.e12935~ (2010)
- Cao C, "SIRT1confers protection against UVB- and H2O2-induced cell death via modulation of p53 and JNK in cultured skin keratinocytes", J. Cell. Mol. Med, 13(9B), pp.3632~3643 (2009)
- Chae HJ, "Sodium nitroprusside induces apoptosis of H9C2 cardiac muscle cells in a c-Jun N-terminal kinase-dependent manner", Int. Immunopharmacol, 1(5), pp.967~978 (2001)
- Chen RM, "Nitric oxide induces osteoblast apoptosis through the de novo synthesis of Bax protein", J Orthop Res, 20(2), pp.295~302 (2002)
- Deliconstantinos G, "Release by ultraviolet B (u.v.B) radiation of nitric oxide (NO) from human keratinocytes:a potential role for nitric oxide in erythema production", Br. J. Pharmacol, 114(6), pp.1257~1265 (1995)
- Kawahara K, "Induction of CHOP and apoptosis by nitric oxide in p53-deficient microglial cells", FEBS Lett, 506(2), pp.135~139 (2001)
- Herbert KJ, "SIRT1 inhibition restores apoptotic sensitivity in p-53 mutated human keratinocytes", Toxicol. Appl. Pharmacol, 277, pp.288~297 (2014)
- Hughes KJ, "FoxO1 and SIRT1Regulate -Cell Responses to Nitric Oxide", J. Biol. Chem, 286, pp.8338~8348 (2011)
- Luo J, "Negative control of p53 by Sir2 promotes cell survival under stress", Cell, 107, pp.137~148 (2001)
- Messmer UK, "Nitric oxide-induced apoptosis: p53-dependent and p53-independent signalling pathways", Biochem. J, 319, pp.299~305 (1995)
- Oyadomari S, "Nitric oxide-induced apoptosis in pancreatic β cells is mediated by the endoplasmic reticulum stress pathway", Proc Natl Acad Sci USA, 98(19), pp.10845~10850 (2001)
- Romero-Graillet C, "Nitric Oxide Produced by Ultraviolet-irradiated Keratinocytes Stimulates Melanogenesis", J, Clin. Invest, 99(4), pp.635~642 (1997)
- Spitler R, "Nitrosyl-cobinamide (NO-Cbi), a new nitric oxide donor, improves wound healing through cGMP", cGMP-dependent protein kinase, 2013, pp.25, 2374~2382
- Takada K, "Endoplasmic reticulum stress mediates nitric oxide-induced chondrocyte apoptosis", Biomed Rep, 1(2), pp.315~319 (2013)
- Weller R, "Autologous nitric oxide protects mouse and human keratinocytes form ultraviolet B radiation-induced apoptosis", Am J Physiol Cell Physiol, 284, pp.1140~1148 (2003)
- Yeung F, "Modulation of NF-κB-dependent transcription and cell survival by the SIRT1 deacetylase", EMBO J, 23, pp.2369~2380 (2004)
- Zhan R, "Nitric oxide enhances keratinocyte cell migration by regulating Rho GTPase via cGMP-PKG signalling", PLoS One, 10(3), pp.e0121551~ (2015)