Evaluation of the Effect of Low Dose of Methamphetamine on the Human Astrocyte Cell Cycle Exposed to Amyloid Beta

Subject Areas : Journal of Animal Biology

Bita Soltanian ¹ ( Department of Biology, Islamic Azad University, Damghan Branch, Damghan, Iran )
Marzieh Dehghan Shasaltaneh ² ( Department of Biology, Faculty of Science, University of Zanjan, Zanjan, Iran )
Gholam Hossein Riazi ³ ( Laboratory of Neuro-Organic Chemistry, Institute of Biochemistry and Biophysics (IBB), University of Tehran, Tehran, Iran )
Nahid Masoudian ⁴ ( Department of Biology, Islamic Azad University, Damghan Branch, Damghan, Iran )

Received: 2021-08-01 Accepted : 2021-08-11 Published : 2022-08-23

Keywords: Methamphetamine, Cell Cycle, Astrocyte, Cyclin Kinase 1, Cyclin E2,

Abstract :

Astrocytes are the most important and abundant cells helping neurons. They are involved in the neural survival, ionic, and osmotic homeostasis, as well as in the formation of synapses and growth of the axons and dendrites. Activating markers of the cell cycle increased in Alzheimer’s disease. Cyclin dependent kinase 1(Cdk1) and cyclin E2 (CE2) are among the cell cycle markers. Besides, methamphetamine in non-toxic dose reduces the automatic division capacity and leads to cell differentiation. In this study, the human astrocytes exposed to amyloid beta (Aβ) and treated with low doses of methamphetamine (METH) and the cell cycle arrest and expression of the Cdk1 and CE2 were assessed in all groups. Five groups were used: 1- The cells expose to Aβ, 2- The cells exposed to METH, 3- The cells exposed to Aβ and then METH, 4- the cells exposed to METH and then Aβ, 5- The control group. Each group was repeated three times. Cdk1 gene expression decreased in group 3, treatment group, but increased in group 4, prevention group. The CE2 gene expression decreased in both groups. Furthermore, the cell cycle arrest in G1, G2, and S were assessed. In the Group 3, treatment group, G2 decreased; but in group 4, prevention group, it increased. Changes in the cell cycle are the early symptoms of Alzheimer’s disease. The low dose of METH can reduce cell cycle activating markers as well as reducing cell division and leading the cells to death.

References:

1. Azzopardi M., Farrugia G., Balzan R., 2017. Cell-cycle involvement in autophagy and apoptosis in yeast. Mechanisms of Ageing and Development, 161: 211-224.


2. Bancher C., Brunner C., Lassmann H. 1989. Accumulation of abnormally phosphorylated τ precedes the formation of neurofibrillary tangles in Alzheimer's disease. Brain Research, 477: 90-99.


3. Baptista S., Lasgi C., Benstaali C., 2014. Methamphetamine decreases dentate gyrus stem cell self-renewal and shifts the differentiation towards neuronal fate. Stem Cell Research, 13: 329-341.


4. Baumann K., Mandelkow E-M, Biernat J., 1993. Abnormal Alzheimer‐like phosphorylation of tau‐protein by cyclin‐dependent kinases cdk2 and cdk5. FEBS Letters, 336: 417-424.


5. Soltanian B., Dehghan Shasaltaneh M., Riazi G., Masoudian N., 2022. The Effective Doses Of METH For Evaluation The Extracellular Glutamine In The Reactive Astrocytes Induced By Aβ. Cell Journal, 24(3): 98.


6. Soltanian B., Dehghan Shasaltaneh M., Riazi G., Masoudian N., 2021. Alteration of Gene Expression in Reactive Astrocytes Induced by Aβ1-42 Using Low Dose of Methamphetamine. Molecular Biology Reports, 48(8): 6103-6112


7. Boonstra J., 2003. Progression through the G1‐phase of the on‐going cell cycle. Journal of Cellular Biochemistry, 90: 244-252.


8. Bowser R., Smith M.A., 2002. Cell cycle proteins in Alzheimer's disease: plenty of wheels but no cycle. Journal of Alzheimer's Disease, 4(3): 249-254.


9. Coqueret O. 2002. Linking cyclins to transcriptional control. Gene, 299: 35-55.


10. Cruz J.C., Tsai L.H., 2004. Cdk5 deregulation in the pathogenesis of Alzheimer's disease. Trends in Molecular Medicine, 10: 452-458.


11. Eckert A., Keil U., Marques C.A., 2003. Mitochondrial dysfunction, apoptotic cell death, and Alzheimer’s disease. Biochemical Pharmacology, 66: 1627-1634.


12. Gerst J.L., Raina A.K., Pirim I. 2000. Altered cell‐matrix associated ADAM proteins in Alzheimer disease. Journal of Neuroscience Research, 59: 680-684.


13. Harguindey S., Reshkin S.J., Orive G. 2007. Growth and trophic factors, pH and the Na+/H+ exchanger in Alzheimer's disease, other neurodegenerative diseases and cancer: new therapeutic possibilities and potential dangers. Current Alzheimer Research, 4: 53-65.


14. Hernández‐Ortega K., Ferrera P., Arias C. 2007. Sequential expression of cell‐cycle regulators and Alzheimer's disease–related proteins in entorhinal cortex after hippocampal excitotoxic damage. Journal of Neuroscience Research, 85: 1744-1751.


15. Hoozemans J.J., Brückner M.K., Rozemuller A.J. 2002. Cyclin D1 and cyclin E are co-localized with cyclo-oxygenase 2 (COX-2) in pyramidal neurons in Alzheimer disease temporal cortex. Journal of Neuropathology and Experimental Neurology, 61: 678-688.


16. Kang Y., Na D.L., Hahn S., 1997. A validity study on the Korean Mini-Mental State Examination (K-MMSE) in dementia patients. Journal of the Korean Neurological Association, 15: 300-308.


17. Kim H., Kwon Y.A., Ahn I.S. 2016. Overexpression of cell cycle proteins of peripheral lymphocytes in patients with Alzheimer's disease. Psychiatry Investigation, 13: 127-134.


18. Marlier Q., Jibassia F., Verteneuil S. 2018. Genetic and pharmacological inhibition of Cdk1 provides neuroprotection towards ischemic neuronal death. Cell Death Discovery, 4: 1-12.


19. McShea A., Lee H.G., Petersen R.B. 2007. Neuronal cell cycle re-entry mediates Alzheimer disease-type changes. Biochimica et Biophysica Acta (BBA).Molecular Basis of Disease, 1772: 467-472.


20. Moh C., Kubiak J.Z., Bajic V.P., 2011. Cell cycle deregulation in the neurons of Alzheimer’s disease. Cell Cycle in Development, 565-576.


21. Nagy Z., Esiri M., Smith A., 1998. The cell division cycle and the pathophysiology of Alzheimer's disease. Neuroscience, 87: 731-739.


22. Noble W., Olm V., Takata K. 2003. Cdk5 is a key factor in tau aggregation and tangle formation in vivo. Neuron, 38: 555-565.


23. Odajima J., Wills Z.P., Ndassa Y.M., 2011. Cyclin E constrains Cdk5 activity to regulate synaptic plasticity and memory formation. Developmental Cell, 21: 655-668.


24. P Silva A., Martins T., Baptista S., 2010. Brain injury associated with widely abused amphetamines: neuroinflammation, neurogenesis and blood-brain barrier. Current drug Abuse Reviews, 3: 239-254


25. Pogocki D. 2002. Alzheimer's beta-amyloid peptide as a source of neurotoxic free radicals: the role of structural effects. Acta Neurobiologiae Experimentalis, 63: 131-146.


26. Raina A.K., Monteiro M.J., Mcshea A., 1999. The role of cell cycle‐mediated events in Alzheimer's disease. International Journal of Experimental Pathology, 80: 71-76.


27. Raina AK., Zhu X., Rottkamp C.A., 2000. Cyclin'toward dementia: cell cycle abnormalities and abortive oncogenesis in Alzheimer disease. Journal of Neuroscience research, 61: 128-133


28. Sánchez I., Dynlacht BD., 2005. New insights into cyclins, CDKs, and cell cycle control. Seminars in Cell and Developmental Biology, 16: 311-321.


29. Thompson PM., Hayashi K.M., Simon S.L., 2004. Structural abnormalities in the brains of human subjects who use methamphetamine. Journal of Neuroscience, 24: 6028-6036.


30. Wojsiat J., Prandelli C., Laskowska-Kaszub K., 2015. Oxidative stress and aberrant cell cycle in Alzheimer’s disease lymphocytes: diagnostic prospects. Journal of Alzheimer's Disease, 46:329-350.


31. Yang Y., Mufson EJ., Herrup K., 2003. Neuronal cell death is preceded by cell cycle events at all stages of Alzheimer's disease. Journal of Neuroscience, 23: 2557-2563.