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Okadaic acid induces JNK activation, bim overexpression and mitochondrial dysfunction in cultured rat cortical neurons.
Neurosci Lett 2006; 394(3):190-5NL

Abstract

Apoptosis via tau phosphorylation has been implicated in the selective neuronal losses seen in Alzheimer's disease (AD). Previous studies in vivo and in cultured neurons have shown that okadaic acid (OA) evokes tau phosphorylation to initiate a neurodegeneration that resembles the pathogenesis of AD. In an effort to identify additional key molecules in this neurodegeneration, we treated cultured rat neurons with OA and examined the apoptosis-related effects, such as changes in mitochondrial activity and expression levels of JNK, Bim, Bad, Bax and caspase-3. Western blotting revealed that phosphorylation of JNK and c-jun occurred first, followed by increased expression of Bim and subsequent caspase-3 activation in OA-treated neurons. In contrast, Bad levels decreased as early as 4 h after OA treatment. Immunocytochemistry showed that the increased phospho-JNK immunoreactivity was localized in the cytosol of degenerating neurons, while increased phospho-c-jun was localized in the nucleus. The mitochondria showed decreased membrane potential and increased swelling after OA treatment. Collectively, these data suggest that JNK- and Bim-related mitochondrial dysfunction is involved in OA-induced neurodegeneration.

Authors+Show Affiliations

Department of Anatomy and Cell Biology, University of Ulsan College of Medicine, 388-1 PoongNap-Dong, SongPa-Gu, Seoul 138-736, Korea.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

16260088

Citation

Yoon, SeungYong, et al. "Okadaic Acid Induces JNK Activation, Bim Overexpression and Mitochondrial Dysfunction in Cultured Rat Cortical Neurons." Neuroscience Letters, vol. 394, no. 3, 2006, pp. 190-5.
Yoon S, Choi J, Yoon J, et al. Okadaic acid induces JNK activation, bim overexpression and mitochondrial dysfunction in cultured rat cortical neurons. Neurosci Lett. 2006;394(3):190-5.
Yoon, S., Choi, J., Yoon, J., Huh, J. W., & Kim, D. (2006). Okadaic acid induces JNK activation, bim overexpression and mitochondrial dysfunction in cultured rat cortical neurons. Neuroscience Letters, 394(3), pp. 190-5.
Yoon S, et al. Okadaic Acid Induces JNK Activation, Bim Overexpression and Mitochondrial Dysfunction in Cultured Rat Cortical Neurons. Neurosci Lett. 2006 Feb 20;394(3):190-5. PubMed PMID: 16260088.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Okadaic acid induces JNK activation, bim overexpression and mitochondrial dysfunction in cultured rat cortical neurons. AU - Yoon,SeungYong, AU - Choi,JungEun, AU - Yoon,JuHee, AU - Huh,Jae-Wan, AU - Kim,DongHou, Y1 - 2005/11/02/ PY - 2005/09/02/received PY - 2005/10/10/revised PY - 2005/10/12/accepted PY - 2005/11/2/pubmed PY - 2006/3/31/medline PY - 2005/11/2/entrez SP - 190 EP - 5 JF - Neuroscience letters JO - Neurosci. Lett. VL - 394 IS - 3 N2 - Apoptosis via tau phosphorylation has been implicated in the selective neuronal losses seen in Alzheimer's disease (AD). Previous studies in vivo and in cultured neurons have shown that okadaic acid (OA) evokes tau phosphorylation to initiate a neurodegeneration that resembles the pathogenesis of AD. In an effort to identify additional key molecules in this neurodegeneration, we treated cultured rat neurons with OA and examined the apoptosis-related effects, such as changes in mitochondrial activity and expression levels of JNK, Bim, Bad, Bax and caspase-3. Western blotting revealed that phosphorylation of JNK and c-jun occurred first, followed by increased expression of Bim and subsequent caspase-3 activation in OA-treated neurons. In contrast, Bad levels decreased as early as 4 h after OA treatment. Immunocytochemistry showed that the increased phospho-JNK immunoreactivity was localized in the cytosol of degenerating neurons, while increased phospho-c-jun was localized in the nucleus. The mitochondria showed decreased membrane potential and increased swelling after OA treatment. Collectively, these data suggest that JNK- and Bim-related mitochondrial dysfunction is involved in OA-induced neurodegeneration. SN - 0304-3940 UR - https://www.unboundmedicine.com/medline/citation/16260088/Okadaic_acid_induces_JNK_activation_bim_overexpression_and_mitochondrial_dysfunction_in_cultured_rat_cortical_neurons_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0304-3940(05)01194-8 DB - PRIME DP - Unbound Medicine ER -