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Arachidonic acid-induced apoptosis of human neuroblastoma SK-N-SH cells is mediated through mitochondrial alteration elicited by ROS and Ca(2+)-evoked activation of p38alpha MAPK and JNK1.
Toxicology. 2009 Aug 21; 262(3):199-206.T

Abstract

Arachidonic acid (AA)-induced apoptosis of human neuroblastoma SK-N-SH cells was characteristic of elevation of intracellular Ca(2+) concentration ([Ca(2+)]i), ROS generation, activation of 38 MAPK and JNK and loss of mitochondrial membrane potential (DeltaPsim). Subsequent modulation of Bcl-2 family members and cytochrome c release accompanied with activation of caspase-9 and -3 were involved in the death of SK-N-SH cells. BAPTA-AM (Ca(2+) chelator) pretreatment rescued viability of AA-treated cells through abolishing phosphorylation of p38 MAPK and JNK, DeltaPsim loss and ROS generation. N-Acetylcysteine (ROS scavenger) pretreatment reduced the dissipation of DeltaPsim, but insignificantly affected AA-induced p38 MAPK and JNK activation. SB202190 (p38 MAPK inhibitor) and SP600125 (JNK inhibitor) attenuated mitochondrial depolarization, degradation of Bcl-2/Bcl-xL, and mitochondrial translocation of Bax. Transfection of specific siRNA proved that p38alpha MAPK and JNK1 were involved in modulating Bcl-2 family proteins. Taken together, our data suggest that the cytotoxicity of AA toward SK-N-SH cells is mediated through mitochondria-dependent death pathway, eliciting by AA-induced ROS generation and Ca(2+)-evoked activation of p38alpha MAPK and JNK1.

Authors+Show Affiliations

Institute of Biomedical Sciences, National Sun Yat-Sen University-Kaohsiung Medical University Joint Research Center, National Sun Yat-Sen University, Kaohsiung 804, Taiwan.No affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19540902

Citation

Chen, Ku-Chung, and Long-Sen Chang. "Arachidonic Acid-induced Apoptosis of Human Neuroblastoma SK-N-SH Cells Is Mediated Through Mitochondrial Alteration Elicited By ROS and Ca(2+)-evoked Activation of P38alpha MAPK and JNK1." Toxicology, vol. 262, no. 3, 2009, pp. 199-206.
Chen KC, Chang LS. Arachidonic acid-induced apoptosis of human neuroblastoma SK-N-SH cells is mediated through mitochondrial alteration elicited by ROS and Ca(2+)-evoked activation of p38alpha MAPK and JNK1. Toxicology. 2009;262(3):199-206.
Chen, K. C., & Chang, L. S. (2009). Arachidonic acid-induced apoptosis of human neuroblastoma SK-N-SH cells is mediated through mitochondrial alteration elicited by ROS and Ca(2+)-evoked activation of p38alpha MAPK and JNK1. Toxicology, 262(3), 199-206. https://doi.org/10.1016/j.tox.2009.06.009
Chen KC, Chang LS. Arachidonic Acid-induced Apoptosis of Human Neuroblastoma SK-N-SH Cells Is Mediated Through Mitochondrial Alteration Elicited By ROS and Ca(2+)-evoked Activation of P38alpha MAPK and JNK1. Toxicology. 2009 Aug 21;262(3):199-206. PubMed PMID: 19540902.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Arachidonic acid-induced apoptosis of human neuroblastoma SK-N-SH cells is mediated through mitochondrial alteration elicited by ROS and Ca(2+)-evoked activation of p38alpha MAPK and JNK1. AU - Chen,Ku-Chung, AU - Chang,Long-Sen, Y1 - 2009/06/21/ PY - 2009/05/12/received PY - 2009/06/10/revised PY - 2009/06/11/accepted PY - 2009/6/23/entrez PY - 2009/6/23/pubmed PY - 2009/8/14/medline SP - 199 EP - 206 JF - Toxicology JO - Toxicology VL - 262 IS - 3 N2 - Arachidonic acid (AA)-induced apoptosis of human neuroblastoma SK-N-SH cells was characteristic of elevation of intracellular Ca(2+) concentration ([Ca(2+)]i), ROS generation, activation of 38 MAPK and JNK and loss of mitochondrial membrane potential (DeltaPsim). Subsequent modulation of Bcl-2 family members and cytochrome c release accompanied with activation of caspase-9 and -3 were involved in the death of SK-N-SH cells. BAPTA-AM (Ca(2+) chelator) pretreatment rescued viability of AA-treated cells through abolishing phosphorylation of p38 MAPK and JNK, DeltaPsim loss and ROS generation. N-Acetylcysteine (ROS scavenger) pretreatment reduced the dissipation of DeltaPsim, but insignificantly affected AA-induced p38 MAPK and JNK activation. SB202190 (p38 MAPK inhibitor) and SP600125 (JNK inhibitor) attenuated mitochondrial depolarization, degradation of Bcl-2/Bcl-xL, and mitochondrial translocation of Bax. Transfection of specific siRNA proved that p38alpha MAPK and JNK1 were involved in modulating Bcl-2 family proteins. Taken together, our data suggest that the cytotoxicity of AA toward SK-N-SH cells is mediated through mitochondria-dependent death pathway, eliciting by AA-induced ROS generation and Ca(2+)-evoked activation of p38alpha MAPK and JNK1. SN - 1879-3185 UR - https://www.unboundmedicine.com/medline/citation/19540902/Arachidonic_acid_induced_apoptosis_of_human_neuroblastoma_SK_N_SH_cells_is_mediated_through_mitochondrial_alteration_elicited_by_ROS_and_Ca_2+__evoked_activation_of_p38alpha_MAPK_and_JNK1_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0300-483X(09)00308-4 DB - PRIME DP - Unbound Medicine ER -