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Acetylcholine inhibits long-term hypoxia-induced apoptosis by suppressing the oxidative stress-mediated MAPKs activation as well as regulation of Bcl-2, c-IAPs, and caspase-3 in mouse embryonic stem cells.
Apoptosis. 2008 Feb; 13(2):295-304.A

Abstract

This study examined the effect of acetylcholine (ACh) on the hypoxia-induced apoptosis of mouse embryonic stem (ES) cells. Hypoxia (60 h) decreased both the cell viability and level of [3H] thymidine incorporation, which were prevented by a pretreatment with ACh. However, the atropine (ACh receptor [AChR] inhibitor) treatment blocked the protective effect of ACh. Hypoxia (90 min) increased the intracellular level of reactive oxygen species (ROS). On the other hand, ACh inhibited the hypoxia-induced increase in ROS, which was blocked by an atropine treatment. Subsequently, the hypoxia-induced ROS increased the level of p38 mitogen activated protein kinase (MAPK) and Jun-N-terminal kinase (JNK) phosphorylation, which were inhibited by the ACh pretreatment. Moreover, hypoxic exposure (90 min) increased the level of nuclear factor-kappa B (NF-kappa B) phosphorylation, which was blocked by a pretreatment with SB 203580 (p38 MAPK inhibitor) or SP 600125 (JNK inhibitor). However, hypoxia (60 h) decreased the protein levels of Bcl-2 and c-IAPs (cellular inhibitor of apoptosis proteins) but increased the level of caspase-3 activation. All these effects were inhibited by a pretreatment with ACh. In conclusion, ACh prevented the hypoxia-induced apoptosis of mouse ES cells by inhibiting the ROS-mediated p38 MAPK and JNK activation as well as the regulation of Bcl-2, c-IAPs, and caspase-3.

Authors+Show Affiliations

Department of Rehabilitation Science, Graduate school of Daegu University, Daegu 705-714, 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

18049903

Citation

Kim, Min Hee, et al. "Acetylcholine Inhibits Long-term Hypoxia-induced Apoptosis By Suppressing the Oxidative Stress-mediated MAPKs Activation as Well as Regulation of Bcl-2, c-IAPs, and Caspase-3 in Mouse Embryonic Stem Cells." Apoptosis : an International Journal On Programmed Cell Death, vol. 13, no. 2, 2008, pp. 295-304.
Kim MH, Kim MO, Heo JS, et al. Acetylcholine inhibits long-term hypoxia-induced apoptosis by suppressing the oxidative stress-mediated MAPKs activation as well as regulation of Bcl-2, c-IAPs, and caspase-3 in mouse embryonic stem cells. Apoptosis. 2008;13(2):295-304.
Kim, M. H., Kim, M. O., Heo, J. S., Kim, J. S., & Han, H. J. (2008). Acetylcholine inhibits long-term hypoxia-induced apoptosis by suppressing the oxidative stress-mediated MAPKs activation as well as regulation of Bcl-2, c-IAPs, and caspase-3 in mouse embryonic stem cells. Apoptosis : an International Journal On Programmed Cell Death, 13(2), 295-304.
Kim MH, et al. Acetylcholine Inhibits Long-term Hypoxia-induced Apoptosis By Suppressing the Oxidative Stress-mediated MAPKs Activation as Well as Regulation of Bcl-2, c-IAPs, and Caspase-3 in Mouse Embryonic Stem Cells. Apoptosis. 2008;13(2):295-304. PubMed PMID: 18049903.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Acetylcholine inhibits long-term hypoxia-induced apoptosis by suppressing the oxidative stress-mediated MAPKs activation as well as regulation of Bcl-2, c-IAPs, and caspase-3 in mouse embryonic stem cells. AU - Kim,Min Hee, AU - Kim,Mi Ok, AU - Heo,Jung Sun, AU - Kim,Jin Sang, AU - Han,Ho Jae, PY - 2007/12/1/pubmed PY - 2008/6/5/medline PY - 2007/12/1/entrez SP - 295 EP - 304 JF - Apoptosis : an international journal on programmed cell death JO - Apoptosis VL - 13 IS - 2 N2 - This study examined the effect of acetylcholine (ACh) on the hypoxia-induced apoptosis of mouse embryonic stem (ES) cells. Hypoxia (60 h) decreased both the cell viability and level of [3H] thymidine incorporation, which were prevented by a pretreatment with ACh. However, the atropine (ACh receptor [AChR] inhibitor) treatment blocked the protective effect of ACh. Hypoxia (90 min) increased the intracellular level of reactive oxygen species (ROS). On the other hand, ACh inhibited the hypoxia-induced increase in ROS, which was blocked by an atropine treatment. Subsequently, the hypoxia-induced ROS increased the level of p38 mitogen activated protein kinase (MAPK) and Jun-N-terminal kinase (JNK) phosphorylation, which were inhibited by the ACh pretreatment. Moreover, hypoxic exposure (90 min) increased the level of nuclear factor-kappa B (NF-kappa B) phosphorylation, which was blocked by a pretreatment with SB 203580 (p38 MAPK inhibitor) or SP 600125 (JNK inhibitor). However, hypoxia (60 h) decreased the protein levels of Bcl-2 and c-IAPs (cellular inhibitor of apoptosis proteins) but increased the level of caspase-3 activation. All these effects were inhibited by a pretreatment with ACh. In conclusion, ACh prevented the hypoxia-induced apoptosis of mouse ES cells by inhibiting the ROS-mediated p38 MAPK and JNK activation as well as the regulation of Bcl-2, c-IAPs, and caspase-3. SN - 1360-8185 UR - https://www.unboundmedicine.com/medline/citation/18049903/Acetylcholine_inhibits_long_term_hypoxia_induced_apoptosis_by_suppressing_the_oxidative_stress_mediated_MAPKs_activation_as_well_as_regulation_of_Bcl_2_c_IAPs_and_caspase_3_in_mouse_embryonic_stem_cells_ L2 - https://doi.org/10.1007/s10495-007-0160-y DB - PRIME DP - Unbound Medicine ER -