Tags

Type your tag names separated by a space and hit enter

Major role of the PI3K/Akt pathway in ischemic tolerance induced by sublethal oxygen-glucose deprivation in cortical neurons in vitro.
Arch Pharm Res. 2011 Jun; 34(6):1023-34.AP

Abstract

Ischemic preconditioning can provide protection to neurons from subsequent lethal ischemia. The molecular mechanisms of neuronal ischemic tolerance, however, are still not well-known. The present study, therefore, examined the role of MAPK and PI3K/Akt pathways in ischemic tolerance induced by preconditioning with sublethal oxygen-glucose deprivation (OGD) in cultured rat cortical neurons. Ischemic tolerance was simulated by preconditioning of the neurons with sublethal 1-h OGD imposed 12 h before lethal 3-h OGD. The time-course studies of relative phosphorylation and expression levels of ERK1/2, JNK and p38 MAPK showed lack of their involvement in ischemic tolerance. However, there were significant increases in Akt phosphorylation levels during the reperfusion period following preconditioned lethal OGD. In addition, Bcl-2 associated death promoter (Bad) and GSK-3β were also found to be inactivated during that reperfusion period. Finally, treatment with an inhibitor of PI3K, wortmannin, applied from 15 min before and during lethal OGD abolished not only the preconditioning-induced neuroprotection but also the Akt activation. Concomitant with blockade of the Akt activation, PI3K inhibition also resulted in activation of Bad and GSK-3β. The results suggest that ischemic tolerance induced by sublethal OGD preconditioning is primarily mediated through activation of the PI3K/Akt pathway, but not the MAPK pathway, in rat cortical neurons.

Authors+Show Affiliations

Integrated Omics Center, Life/Health Division, Korea Institute of Science and Technology (KIST), P.O. Box 131, Cheongryang, Seoul 130-650, 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

21725824

Citation

Bhuiyan, Mohammad Iqbal Hossain, et al. "Major Role of the PI3K/Akt Pathway in Ischemic Tolerance Induced By Sublethal Oxygen-glucose Deprivation in Cortical Neurons in Vitro." Archives of Pharmacal Research, vol. 34, no. 6, 2011, pp. 1023-34.
Bhuiyan MI, Jung SY, Kim HJ, et al. Major role of the PI3K/Akt pathway in ischemic tolerance induced by sublethal oxygen-glucose deprivation in cortical neurons in vitro. Arch Pharm Res. 2011;34(6):1023-34.
Bhuiyan, M. I., Jung, S. Y., Kim, H. J., Lee, Y. S., & Jin, C. (2011). Major role of the PI3K/Akt pathway in ischemic tolerance induced by sublethal oxygen-glucose deprivation in cortical neurons in vitro. Archives of Pharmacal Research, 34(6), 1023-34. https://doi.org/10.1007/s12272-011-0620-3
Bhuiyan MI, et al. Major Role of the PI3K/Akt Pathway in Ischemic Tolerance Induced By Sublethal Oxygen-glucose Deprivation in Cortical Neurons in Vitro. Arch Pharm Res. 2011;34(6):1023-34. PubMed PMID: 21725824.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Major role of the PI3K/Akt pathway in ischemic tolerance induced by sublethal oxygen-glucose deprivation in cortical neurons in vitro. AU - Bhuiyan,Mohammad Iqbal Hossain, AU - Jung,Seo Yun, AU - Kim,Hyoung Ja, AU - Lee,Yong Sup, AU - Jin,Changbae, Y1 - 2011/07/02/ PY - 2010/09/30/received PY - 2011/02/24/accepted PY - 2011/01/30/revised PY - 2011/7/5/entrez PY - 2011/7/5/pubmed PY - 2011/11/1/medline SP - 1023 EP - 34 JF - Archives of pharmacal research JO - Arch Pharm Res VL - 34 IS - 6 N2 - Ischemic preconditioning can provide protection to neurons from subsequent lethal ischemia. The molecular mechanisms of neuronal ischemic tolerance, however, are still not well-known. The present study, therefore, examined the role of MAPK and PI3K/Akt pathways in ischemic tolerance induced by preconditioning with sublethal oxygen-glucose deprivation (OGD) in cultured rat cortical neurons. Ischemic tolerance was simulated by preconditioning of the neurons with sublethal 1-h OGD imposed 12 h before lethal 3-h OGD. The time-course studies of relative phosphorylation and expression levels of ERK1/2, JNK and p38 MAPK showed lack of their involvement in ischemic tolerance. However, there were significant increases in Akt phosphorylation levels during the reperfusion period following preconditioned lethal OGD. In addition, Bcl-2 associated death promoter (Bad) and GSK-3β were also found to be inactivated during that reperfusion period. Finally, treatment with an inhibitor of PI3K, wortmannin, applied from 15 min before and during lethal OGD abolished not only the preconditioning-induced neuroprotection but also the Akt activation. Concomitant with blockade of the Akt activation, PI3K inhibition also resulted in activation of Bad and GSK-3β. The results suggest that ischemic tolerance induced by sublethal OGD preconditioning is primarily mediated through activation of the PI3K/Akt pathway, but not the MAPK pathway, in rat cortical neurons. SN - 0253-6269 UR - https://www.unboundmedicine.com/medline/citation/21725824/Major_role_of_the_PI3K/Akt_pathway_in_ischemic_tolerance_induced_by_sublethal_oxygen_glucose_deprivation_in_cortical_neurons_in_vitro_ L2 - https://dx.doi.org/10.1007/s12272-011-0620-3 DB - PRIME DP - Unbound Medicine ER -