Study of relationship between Tau protein changes and glutamate expression in basal ganglia after hypoxic-ischemic reperfusion injury in piglets

ZHENG Yang; WANG Xiao-ming

doi:10.12117/jccmi.2018.08.004

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Journal of China Clinic Medical Imaging ›› 2018, Vol. 29 ›› Issue (8) : 543-547. DOI: 10.12117/jccmi.2018.08.004

Study of relationship between Tau protein changes and glutamate expression in basal ganglia after hypoxic-ischemic reperfusion injury in piglets

ZHENG Yang, WANG Xiao-ming

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Abstract

Objective: To investigate the Tau protein expression and glutamate(Glu) characteristics in basal ganglia following hypoxic-ischemic(HI) reperfusion brain injury in a piglet model, further defined the Tau protein and Glu in the role of HI brain injury mechanism. Methods: A total of 45 healthy piglets(3~5 days old, 1.0~1.5 kg) were divided into control(n=9) and hypoxic-ischemic(HI) model groups(n=36). The HI model group was further divided into six groups according to 1H-magnetic resonance spectroscopy(1H-MRS) scan times after HI(0~2 h, 2~6 h, 6~12 h, 12~24 h, 24~48 h and 48~72 h). Measure Tau protein and Glu at different time points after HI in basal ganglia and the correlation of Tau protein and Glu, P<0.05 considered statistically significant, the decimal to 2 digits. Results: The results of 1H-MRS showed that after HI, the Tau protein content increased first, then decreased, and reached the highest point in 24~48 h, which was statistically different from the control group. Glu appears to rise first, then decreases, then rises again, showing a “bimodal” change, which peaks at 6~12 h and 24~48 h. Tau protein and Glu were positively correlated, correlation coefficient r=0.76(P<0.05). Conclusions: These results indicate that after HI, Tau protein and Glu work together on the neural networks and neurons and glial cells in the brain.

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Brain injuries / tau proteins / Glutamic acid / Swine, miniature / Magnetic resonance imaging

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ZHENG Yang, WANG Xiao-ming. Study of relationship between Tau protein changes and glutamate expression in basal ganglia after hypoxic-ischemic reperfusion injury in piglets[J]. Journal of China Clinic Medical Imaging. 2018, 29(8): 543-547 https://doi.org/10.12117/jccmi.2018.08.004

References

[1]Sebastián-Serrano A, de Diego-García L, Díaz-Hernández M. The neurotoxic role of extracellular Tau protein[J]. Int J Mol Sci, 2018, 19(4): E998.
[2]Jazvinscak Jembrek M, Slade N, Hof PR, et al. The interactions of p53 with tau and Aβ represent potential therapeutic targets for Alzheimer’s disease[J]. Prog Neurobiol, 2018. [Epub ahead of print]
[3]Wen Y, Yang S, Liu R, et al. Transient cerebral ischemia induces aberrant neuronal cell cycle re-entry and Alzheimer’s disease-like tauopathy in female rats[J]. J Biol Chem, 2004, 279(21): 22684-22692.
[4]Munkeby BH, De Lange C, Emblem KE, et al. A piglet model for detection of hypoxic-ischemic brain injury with magnetic resonance imaging[J]. Acta Radiol, 2008, 49(9): 1049-1057.
[5]LeBlanc MH, Qian XB, Cai ZW. The effect of glucose during ischemia on brain ATP, lactate, and glutamate in piglets[J]. Biol Neonate, 1997, 72(4): 243-254.
[6]Vial F, Serriere S, Barantin L, et al. A newborn piglet study of moderate hypoxic-ischemic brain injury by 1H-MRS and MRI[J]. Magn Reson Imaging, 2004, 22(4): 457-465.
[7]McCulloch KM, Raju TN, Navale S, et al. Developing a long-term surviving piglet model of neonatal hypoxic-ischemic encephalopathy[J]. Neurol Res, 2005, 27(1): 16-21.
[8]Kreis R, Hofmann L, Kuhlmann B, et al. Brain metabolite composition during early human brain development as measured by quantitative in vivo 1H magnetic resonance spectroscopy[J]. Magn Reson Med, 2002, 48(6): 949-958.
[9]Hüppi PS, Posse S, Lazeyras F, et al. Magnetic resonance in preterm and term newborns: 1H-spectroscopy in developing human brain[J]. Pediatr Res, 1991, 30(6): 574-578.
[10]Fiacco TA, McCarthy KD. Intracellular astrocyte calcium waves in situ increase the frequency of spontaneous AMPA receptor currents in CA1 pyramidal neurons[J]. J Neurosci, 2004, 24(3): 722-732.
[11]Fellin T, Pascual O, Gobbo S, et al. Neuronal synchrony mediated by astrocytic glutamate through activation of extrasynaptic NMDA receptors[J]. Neuron, 2004, 43(5): 729-743.
[12]Jourdain P, Bergersen LH, Bhaukaurally K, et al. Glutamate exocytosis from astrocytes controls synaptic strength[J]. Nat Neurosci, 2007, 10(3): 331-339.
[13]Fannon J, Tarmier W, Fulton D. Neuronal activity and AMPA-type glutamate receptor activation regulates the morphological development of oligodendrocyte precursor cells[J]. Glia, 2015, 63(6): 1021-1035.
[14]Liu F, Li B, Tung EJ, et al. Site-specific effects of tau phosphorylation on its microtubule assembly activity and self-aggregation[J]. Eur J Neurosci, 2007, 26(12): 3429-3436.
[15]Wagner U, Utton M, Gallo JM, et al. Cellular phosphorylation of tau by GSK-3 beta influences tau binding to microtubules and microtubule organisation[J]. J Cell Sci, 1996, 109(Pt 6): 1537-1543.
[16]Rissman RA, Lee KF, Vale W, et al. Corticotropin-releasing factor receptors differentially regulate stress-induced tau phosphorylation[J]. J Neurosci, 2007, 27(24): 6552-6562.
[17]Munoz L, Ammit AJ. Targeting p38 MAPK pathway for the treatment of Alzheimer’s disease[J]. Neuropharmacology, 2010, 58(3): 561-568.
[18]Ghosh S, Wu MD, Shaftel SS, et al. Sustained interleukin-1β overexpression exacerbates tau pathology despite reduced amyloid burden in an Alzheimer’s mouse model[J]. J Neurosci, 2013, 33(11): 5053-5064.
[19]Murugan M, Ling EA, Kaur C. Dysregulated glutamate uptake by astrocytes causes oligodendroglia death in hypoxic perventricular white matter damage[J]. Mol Cell Neurosci, 2013, 56: 342-354.
[20]Mallard C, Davidson JO, Tan S, et al. Astrocytes and microglia in acute cerebral injury underlying cerebral palsy associated with preterm birth[J]. Pediatr Res, 2014, 75(1-2): 234-240.
[21]Wallen M, Gillies D. Intra-articular steroids and splints/rest for children with juvenile idiopathic arthritis and adults with rheumatoid arthritis[J]. Cochrane Database Syst Rev, 2006, (1): CD002824.
[22]Liliang PC, Liang CL, Lu K, et al. Relationship between injury severity and serum tau protein levels in traumatic brain injured rats[J]. Resuscitation, 2010, 81(9): 1205-1208.
[23]Sulu B, Cihan M, Gunerhan Y, et al. The healing effect of shark cartilage in rabbits after colonic anastomosis[J]. Ann Ital Chir, 2013, 84(3): 351-356.
[24]Rametti A, Esclaire F, Yardin C, et al. Linking alterations in tau phosphorylation and cleavage during neuronal apoptosis[J]. J Biol Chem, 2004, 279(52): 54518-54528.
[25]Bacci A, Sancini G, Verderio C, et al. Block of glutamate-glutamine cycle between astrocytes and neurons inhibits epileptiform activity in hippocampus[J]. J Neurophysiol, 2002, 88(5): 2302-2310.
[26]Matsumoto K, Lo EH, Pierce AR, et al. Secondary elevation of extracellular neurotransmitter amino acids in the reperfusion phase following focal cerebral ischemia[J]. J Cereb Blood Flow Metab, 1996, 16(1): 114-124.
[27]Franz G, Beer R, Kampfl A, et al. Amyloid beta 1~42 and tau in cerebrospinal fluid after severe traumatic brain injury[J]. Neurology, 2003, 60(9): 1457-1461.