Involvement of TRPM7 calcium channels and PI3K/AKT kinase pathway in protective effect of vascular endothelial growth factor in amyloid beta-induced model of Alzheimer’ s disease

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Mehrabi Jila; Eftekhar Ardebili Mehrdad; Amiri Mona; BALUCHNEJADMOJARAD TOURANDOKHT

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Journal: DANESHVAR MEDICINE Year:2019 | Volume:27 | Issue:141 Page(s): 19-26

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Title

Involvement of TRPM7 calcium channels and PI3K/AKT kinase pathway in protective effect of vascular endothelial growth factor in amyloid beta-induced model of Alzheimer’ s disease

Author(s)

Mehrabi Jila | Eftekhar Ardebili Mehrdad | Amiri Mona | BALUCHNEJADMOJARAD TOURANDOKHT | Issue Writer Certificate

Keywords

Alzheimer’s diseaseQ2

Amyloid betaQ2

Vascular endothelial growth factorQ2

TRPM7 channelQ1

PI3K/AktQ1

Abstract

Background and Objective: Alzheimer’ s disease (AD) is a progressive neurodegenerative disorder, in which cortical and hippocampus neurons death is the main target of neurodegeneration. In addition to extracellular beta amyloid accumulation and the production of neural tangles, one of effective factors in the pathology of Alzheimer's disease is vascular injury in the elderly including disturbance in Vascular endothelial growth factor (VEGF) function. The present study was conducted to investigate the effect of pre-treatment with different concentrations of VEGF in a cellular model of Aβ-induced Alzheimer's disease. Materials and Methods: After culturing and passaging human neuroblastoma cells (SH-SY5Y), they were evaluated in control, control pretreated with different concentrations of VEGF (0. 5, 1 and 2 nM), Amyloid beta, Amyloid beta with the same concentrations of VEGF, and Amyloid beta pretreated with the most effective concentration of VEGF in addition to TRPM7 channels antagonist (2-APB) or AKT inhibitor. For assessment of cell viability, MTT assay was applied. Results: Findings of this study showed that Amyloid beta significantly reduces cell viability (p<0. 001), VEGF pretreatment significantly increases cell viability in a concentration-dependent manner, and this beneficial effect was not observed in the presence of TRPM7 channels antagonist or AKT inhibitor. Conclusion: It is concluded that VEGF could prevent Amyloid beta-induced reduction of cell viability and its beneficial effect is mediated through TRPM7 channels and PI3K/Akt signaling.

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APA: Copy

Mehrabi, Jila, Eftekhar Ardebili, Mehrdad, Amiri, Mona, & BALUCHNEJADMOJARAD, TOURANDOKHT. (2019). Involvement of TRPM7 calcium channels and PI3K/AKT kinase pathway in protective effect of vascular endothelial growth factor in amyloid beta-induced model of Alzheimer’ s disease. DANESHVAR MEDICINE, 27(141 ), 19-26. SID. https://sid.ir/paper/31028/en

Vancouver: Copy

Mehrabi Jila, Eftekhar Ardebili Mehrdad, Amiri Mona, BALUCHNEJADMOJARAD TOURANDOKHT. Involvement of TRPM7 calcium channels and PI3K/AKT kinase pathway in protective effect of vascular endothelial growth factor in amyloid beta-induced model of Alzheimer’ s disease. DANESHVAR MEDICINE[Internet]. 2019;27(141 ):19-26. Available from: https://sid.ir/paper/31028/en

IEEE: Copy

Jila Mehrabi, Mehrdad Eftekhar Ardebili, Mona Amiri, and TOURANDOKHT BALUCHNEJADMOJARAD, “Involvement of TRPM7 calcium channels and PI3K/AKT kinase pathway in protective effect of vascular endothelial growth factor in amyloid beta-induced model of Alzheimer’ s disease,” DANESHVAR MEDICINE, vol. 27, no. 141 , pp. 19–26, 2019, [Online]. Available: https://sid.ir/paper/31028/en

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