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Cx43 Mediates Resistance against MPP⁺-Induced Apoptosis in SH-SY5Y Neuroblastoma Cells via Modulating the Mitochondrial Apoptosis Pathway.
Int J Mol Sci. 2016 Nov 01; 17(11)IJ

Abstract

Neuronal apoptosis in the substantia nigra par compacta (SNpc) appears to play an essential role in the pathogenesis of Parkinson's disease. However, the mechanisms responsible for the death of dopaminergic neurons are not fully understood yet. To explore the apoptotic mechanisms, we used a well-known parkinsonian toxin, 1-methyl-4-phenylpyridine (MPP⁺), to induce neuronal apoptosis in the human dopaminergic SH-SY5Y cell line. The most common method of interaction between cells is gap junctional intercellular communication (GJIC) mediated by gap junctions (GJs) formed by transmembrane proteins called connexins (Cx). Modulation of GJIC affects cell viability or growth, implying that GJIC may have an important role in maintaining homeostasis in various organs. Here, we hypothesized that increasing the level of the gap junction protein Cx43 in SH-SY5Y neuroblastoma cells could provide neuroprotection. First, our experiments demonstrated that knocking down Cx43 protein by using Cx43-specific shRNA in SH-SY5Y neuroblastoma cells potentiated MPP⁺-induced neuronal apoptosis evident from decreased cell viability. In another experiment, we demonstrated that over-expression of Cx43 in the SH-SY5Y cell system decreased MPP⁺-induced apoptosis based on the MTT assay and reduced the Bax/Bcl-2 ratio and the release of cytochrome C based on Western blot analysis. Taken together, our results suggest that Cx43 could mediate resistance against MPP⁺-induced apoptosis in SH-SY5Y neuroblastoma cells via modulating the mitochondrial apoptosis pathway.

Authors+Show Affiliations

Department of Biotechnology, Konkuk University, Chungju 380-701, Korea. kis5497@kku.ac.kr.Nanotechnology Research Center and Department of Applied Life Science, College of Biomedical and Health Science, Konkuk University, Chungju 380-701, Korea. palanivel@kku.ac.kr.Department of Biotechnology, Konkuk University, Chungju 380-701, Korea. choidk@kku.ac.kr.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

27809287

Citation

Kim, In-Su, et al. "Cx43 Mediates Resistance Against MPP⁺-Induced Apoptosis in SH-SY5Y Neuroblastoma Cells Via Modulating the Mitochondrial Apoptosis Pathway." International Journal of Molecular Sciences, vol. 17, no. 11, 2016.
Kim IS, Ganesan P, Choi DK. Cx43 Mediates Resistance against MPP⁺-Induced Apoptosis in SH-SY5Y Neuroblastoma Cells via Modulating the Mitochondrial Apoptosis Pathway. Int J Mol Sci. 2016;17(11).
Kim, I. S., Ganesan, P., & Choi, D. K. (2016). Cx43 Mediates Resistance against MPP⁺-Induced Apoptosis in SH-SY5Y Neuroblastoma Cells via Modulating the Mitochondrial Apoptosis Pathway. International Journal of Molecular Sciences, 17(11).
Kim IS, Ganesan P, Choi DK. Cx43 Mediates Resistance Against MPP⁺-Induced Apoptosis in SH-SY5Y Neuroblastoma Cells Via Modulating the Mitochondrial Apoptosis Pathway. Int J Mol Sci. 2016 Nov 1;17(11) PubMed PMID: 27809287.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Cx43 Mediates Resistance against MPP⁺-Induced Apoptosis in SH-SY5Y Neuroblastoma Cells via Modulating the Mitochondrial Apoptosis Pathway. AU - Kim,In-Su, AU - Ganesan,Palanivel, AU - Choi,Dong-Kug, Y1 - 2016/11/01/ PY - 2016/09/08/received PY - 2016/10/13/revised PY - 2016/10/25/accepted PY - 2016/11/4/pubmed PY - 2017/4/11/medline PY - 2016/11/4/entrez KW - 1-methyl-4-phenylpyridine (MPP+) KW - SH-SY5Y KW - apoptosis KW - connexin 43 KW - mitochondira JF - International journal of molecular sciences JO - Int J Mol Sci VL - 17 IS - 11 N2 - Neuronal apoptosis in the substantia nigra par compacta (SNpc) appears to play an essential role in the pathogenesis of Parkinson's disease. However, the mechanisms responsible for the death of dopaminergic neurons are not fully understood yet. To explore the apoptotic mechanisms, we used a well-known parkinsonian toxin, 1-methyl-4-phenylpyridine (MPP⁺), to induce neuronal apoptosis in the human dopaminergic SH-SY5Y cell line. The most common method of interaction between cells is gap junctional intercellular communication (GJIC) mediated by gap junctions (GJs) formed by transmembrane proteins called connexins (Cx). Modulation of GJIC affects cell viability or growth, implying that GJIC may have an important role in maintaining homeostasis in various organs. Here, we hypothesized that increasing the level of the gap junction protein Cx43 in SH-SY5Y neuroblastoma cells could provide neuroprotection. First, our experiments demonstrated that knocking down Cx43 protein by using Cx43-specific shRNA in SH-SY5Y neuroblastoma cells potentiated MPP⁺-induced neuronal apoptosis evident from decreased cell viability. In another experiment, we demonstrated that over-expression of Cx43 in the SH-SY5Y cell system decreased MPP⁺-induced apoptosis based on the MTT assay and reduced the Bax/Bcl-2 ratio and the release of cytochrome C based on Western blot analysis. Taken together, our results suggest that Cx43 could mediate resistance against MPP⁺-induced apoptosis in SH-SY5Y neuroblastoma cells via modulating the mitochondrial apoptosis pathway. SN - 1422-0067 UR - https://www.unboundmedicine.com/medline/citation/27809287/Cx43_Mediates_Resistance_against_MPP���_Induced_Apoptosis_in_SH_SY5Y_Neuroblastoma_Cells_via_Modulating_the_Mitochondrial_Apoptosis_Pathway_ L2 - https://www.mdpi.com/resolver?pii=ijms17111819 DB - PRIME DP - Unbound Medicine ER -