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HGF protects cultured cortical neurons against hypoxia/reoxygenation induced cell injury via ERK1/2 and PI-3K/Akt pathways.
Colloids Surf B Biointerfaces. 2008 Feb 15; 61(2):290-7.CS

Abstract

Hepatocyte growth factor (HGF) has been revealed to exert multipotent activities on a variety of cells. In this study, we investigated whether HGF had a direct neuroprotection on cultured cerebral cortical neurons subjected to hypoxia/reoxygenation (H/R) and explored the intracellular signalings mediated the effects. The decrease in cell viability and increase in number of apoptotic cells resulting from H/R were significantly prevented by HGF pre-treatment. HGF stimulated both ERK1/2 and Akt activities in cortical neurons. Inhibition of ERK activation completely abolished the protective effects of HGF, and inhibition of Akt activation reduced, but did not completely eliminate the HGF mediated neuroprotection. It is suggested that the neuroprotection of HGF depend on ERK1/2 pathway, and, to a lesser extent, PI-3K/Akt pathway. In addition, we found that pre-treatment with HGF remarkably attenuated the decrease in expression of Bcl-2 and Bcl-xL induced by H/R, but failed to affect the amount of Bax. It is likely that Bcl-2 and Bcl-xL contribute to the protective effects of HGF.

Authors+Show Affiliations

Department of Physiology, Xiangya School of Medicine, Central South University, Changsha 410008, China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo 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

17942284

Citation

He, Fang, et al. "HGF Protects Cultured Cortical Neurons Against Hypoxia/reoxygenation Induced Cell Injury Via ERK1/2 and PI-3K/Akt Pathways." Colloids and Surfaces. B, Biointerfaces, vol. 61, no. 2, 2008, pp. 290-7.
He F, Wu LX, Shu KX, et al. HGF protects cultured cortical neurons against hypoxia/reoxygenation induced cell injury via ERK1/2 and PI-3K/Akt pathways. Colloids Surf B Biointerfaces. 2008;61(2):290-7.
He, F., Wu, L. X., Shu, K. X., Liu, F. Y., Yang, L. J., Zhou, X., Zhang, Y., Huang, B. S., Huang, D., & Deng, X. L. (2008). HGF protects cultured cortical neurons against hypoxia/reoxygenation induced cell injury via ERK1/2 and PI-3K/Akt pathways. Colloids and Surfaces. B, Biointerfaces, 61(2), 290-7.
He F, et al. HGF Protects Cultured Cortical Neurons Against Hypoxia/reoxygenation Induced Cell Injury Via ERK1/2 and PI-3K/Akt Pathways. Colloids Surf B Biointerfaces. 2008 Feb 15;61(2):290-7. PubMed PMID: 17942284.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - HGF protects cultured cortical neurons against hypoxia/reoxygenation induced cell injury via ERK1/2 and PI-3K/Akt pathways. AU - He,Fang, AU - Wu,Li-Xiang, AU - Shu,Kun-Xian, AU - Liu,Fa-Yi, AU - Yang,Li-Juan, AU - Zhou,Xuan, AU - Zhang,Yan, AU - Huang,Bo-Sheng, AU - Huang,Dong, AU - Deng,Xiao-Lu, Y1 - 2007/09/08/ PY - 2007/05/16/received PY - 2007/08/14/revised PY - 2007/09/02/accepted PY - 2007/10/19/pubmed PY - 2008/4/11/medline PY - 2007/10/19/entrez SP - 290 EP - 7 JF - Colloids and surfaces. B, Biointerfaces JO - Colloids Surf B Biointerfaces VL - 61 IS - 2 N2 - Hepatocyte growth factor (HGF) has been revealed to exert multipotent activities on a variety of cells. In this study, we investigated whether HGF had a direct neuroprotection on cultured cerebral cortical neurons subjected to hypoxia/reoxygenation (H/R) and explored the intracellular signalings mediated the effects. The decrease in cell viability and increase in number of apoptotic cells resulting from H/R were significantly prevented by HGF pre-treatment. HGF stimulated both ERK1/2 and Akt activities in cortical neurons. Inhibition of ERK activation completely abolished the protective effects of HGF, and inhibition of Akt activation reduced, but did not completely eliminate the HGF mediated neuroprotection. It is suggested that the neuroprotection of HGF depend on ERK1/2 pathway, and, to a lesser extent, PI-3K/Akt pathway. In addition, we found that pre-treatment with HGF remarkably attenuated the decrease in expression of Bcl-2 and Bcl-xL induced by H/R, but failed to affect the amount of Bax. It is likely that Bcl-2 and Bcl-xL contribute to the protective effects of HGF. SN - 0927-7765 UR - https://www.unboundmedicine.com/medline/citation/17942284/HGF_protects_cultured_cortical_neurons_against_hypoxia/reoxygenation_induced_cell_injury_via_ERK1/2_and_PI_3K/Akt_pathways_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0927-7765(07)00359-1 DB - PRIME DP - Unbound Medicine ER -