Effects of Modeling of Hypercalcemia and β-Amyloid on Cultured Hippocampal Neurons of Rats

1.

Y. N. Tyshchenko and E. A. Lukyanetz, “The role of beta-amyloid in the norm and at Alzheimer`s disease,” Fiziol. Zh., 66, No. 6, 88–96 (2020).

Article  Google Scholar 

2.

B. Fadeel and S. Orrenius, “Apoptosis: a basic biological phenomenon with wide-ranging implications in human disease,” J. intern. Med., 258, No. 6, 479–517 (2005).

CAS  Article  Google Scholar 

3.

P. Kostyuk, E. Lukyanetz, and Ya. Shuba, “Molecular physiology and pharmacology of the calcium channels,” Neurophysiology, 34, Nos. 2–3, 97–101 (2002).

CAS  Article  Google Scholar 

4.

P. G. Kostyk, E. P. Kostyuk, and E. A. Lukyanetz, Intracellular Calcium Signaling – Structures and Functions, Naukova Dumka, Kyiv, 176 p. (2010).

5.

P. G. Kostyk, E. Kostyuk, E. A. Lukyanetz, Calcium Ions in Brain Function – From Physiology to Pathology, Naukova Dumka, Kyiv, 152 p. (2005).

6.

P. G. Kostyuk and E. A. Lukyanetz, “Intracellular calcium signaling – basic mechanisms and possible alterations,” in: Bioelectromagnetics: Current Concepts, S. N. Ayrapetyan, M. S. Markov (eds.), NATO Security through Science Series, Springer, The Netherlands, pp. 87–122 (2006).

7.

P. Goldstein and G. Kroemer, “Cell death by necrosis: towards a molecular definition,” Trends Biochem. Sci., 32, No. 1, 37–43 (2007).

Article  Google Scholar 

8.

N. Festjens, T. Vanden Berghe, and P. Vandenabeele, “Necrosis, a well-orchestrated form of cell demise: signalling cascades, important mediators and concomitant immune response,” Biochim. Biophys. Acta, 1757, Nos. 9–10, 1371–1387 (2006).

CAS  Article  Google Scholar 

9.

W. Wu, P. Liu, and J. Li, “Necroptosis: an emerging form of programmed cell death,” Crit. Rev. Oncol. Hematol., 82, No. 3, 249–258 (2012).

Article  Google Scholar 

10.

Z. S. Khachaturian, “Diagnosis of Alzheimer’s disease,” Arch. Neurol., 42, No. 11, 1097–1105 (1985).

CAS  Article  Google Scholar 

11.

B. D. Arbo, J. B. Hoppe, K. Rodrigues, et al., “4’-Chlorodiazepam is neuroprotective against amyloid-beta in organotypic hippocampal cultures,” J. Steroid Biochem. Mol. Biol., 171, 281–287 (2017).

CAS  Article  Google Scholar 

12.

M. Calvo-Rodriguez, E. Hernando-Perez, L. Nuñez, and C. Villalobos, “Amyloid β oligomers increase ER-mitochondria Ca2+ cross talk in young hippocampal neurons and exacerbate aging-induced intracellular Ca2+ remodeling,” Front. Cell. Neurosci., 13, 22 (2019).

CAS  Article  Google Scholar 

13.

E. V. Kravenska, V. V. Chopovska, E. N. Yavorskaya, et al., “The role of mitochondria in the development of Alzheimer’s disease,” Tavrich. Med. Biol. Bull., 15, No. 3/2, 147–149 (2012).

Google Scholar 

14.

E. V. Kravenska, V. V. Ganzha, E. N. Yavorskaya, and E. A. Lukyanetz, “Effect of cyclosporin A on the viability of hippocampal cells cultured under conditions of modeling of Alzheimer’s disease,” Neurophysiology, 48, No. 4, 246–251 (2016).

CAS  Article  Google Scholar 

15.

S. Beesley, J. Olcese, C. Saunders, and E. A. Bienkiewicz, “Combinatorial treatment effects in a cell culture model of Alzheimer’s disease,” J. Alzheimers Dis., 55, No. 3, 1 155–1166 (2017).

16.

S. K. Dubey, M. S. Ram, K. V. Krishna, et al., “Recent expansions on cellular models to uncover the scientific barriers towards drug development for Alzheimer’s disease,” Cell. Mol. Neurobiol., 39, No. 2, 181–209 (2019).

CAS  Article  Google Scholar 

17.

V. M. Shkryl, P. G. Kostyuk, and E. A. Lukyanetz, “Dual action of cytosolic calcium on calcium channel activity during hypoxia in hippocampal neurones,” Neuroreport, 12, No. 18, 4035–4039 (2001).

CAS  Article  Google Scholar 

18.

V. M. Shkryl, L. M. Nikolaenko, P. G. Kostyuk, and E. A. Lukyanetz, “High-threshold calcium channel activity in rat hippocampal neurones during hypoxia,” Brain Res., 833, No. 2, 319–328 (1999).

CAS  Article  Google Scholar 

19.

V. M. Shkryl, “Error correction due to background subtraction in ratiometric calcium measurements with CCD camera,” Heliyon, 6, No. 6, e04180 (2020).

Article  Google Scholar 

20.

M. S. D’Arcy, “Cell death: a review of the major forms of apoptosis, necrosis and autophagy,” Cell Biol. Int., 43, No. 6, 582–592 (2019).

Article  Google Scholar 

21.

E. Hooshmandi, M. Moosavi, H. Katinger, et al., “CEPO (carbamylated erythropoietin)-Fc protects hippocampal cells in culture against beta amyloid-induced apoptosis: considering Akt/GSK-3β and ERK signaling pathways,” Mol. Biol. Rep., 47, No. 3, 2097–2108 (2020).

CAS  Article  Google Scholar 

22.

E. Hooshmandi, R. Ghasemi, P. Iloun, and M. Moosavi, “The neuroprotective effect of agmatine against amyl-oid β-induced apoptosis in primary cultured hippocampal cells involving ERK, Akt/GSK-3β, and TNF-α,” Mol. Biol. Rep., 46, No. 1, 489–496 (2019).

CAS  Article  Google Scholar 

23.

Z. H. Ji, H. Zhao, C. Liu, and X.-Y. Yu, “In-vitro neuroprotective effect and mechanism of 2β-hydroxy-δ-cadinol against amyloid β-induced neuronal apoptosis,” Neuroreport, 31, No. 3, 245–250 (2020).

CAS  Article  Google Scholar 

24.

T. Y. Korol and O. P. Kostyuk, “Damage of calciumcapturing function of mitochondria in experimental Alzheimer’s disease,” Rep. NAS Ukraine, No. 6, 186–190 (2009).

Google Scholar 

25.

Y. Kravenska, H. Nieznanska, K. Nieznanski, et al., “The monomers, oligomers, and fibrils of amyloid-β inhibit the activity of mitoBKCa channels by a membranemediated mechanism,” Biochim. Biophys. Acta (BBA) Biomembranes, 1862, No. 9,183337 (2020).

CAS  Article  Google Scholar 

26.

O. P. Kostiuk, T. Korol’, S. V. Korol’, et al., “Alteration of calcium signaling as one of the mechanisms of Alzheimer’s disease and diabetic polyneuropathy,” Fiziol. Zh., 56, No. 4, 130–138 (2010).

CAS  Article  Google Scholar 

27.

M. Ramsden, Z. Henderson, and H. A. Pearson, “Modulation of Ca2+ channel currents in primary cultures of rat cortical neurones by amyloid beta protein (1-40) is dependent on solubility status,” Brain Res., 956, No. 2, 254–261 (2002).

CAS  Article  Google Scholar 

28.

D. G. Cook, X. Li, S. D. Cherry, and A. R. Cantrell, “Presenilin 1 deficiency alters the activity of voltagegated Ca2+ channels in cultured cortical neurons,” J. Neurophysiol., 94, No. 6, 4421–4429 (2005).

CAS  Article  Google Scholar 

29.

R. M. Davidson, L. Shajenko, and T. S. Donta, “Amyloid beta-peptide (Abeta P) potentiates a nimodipinesensitive L-type barium conductance in N1E-115 neuroblastoma cells,” Brain Res., 643, Nos. 1–2, 324–327 (1994).

CAS  Article  Google Scholar 

30.

W. Y. Li, J. P. Butler, J. E. Hale, et al., “Suppression of an amyloid beta peptide-mediated calcium channel response by a secreted beta-amyloid precursor protein,” Neuroscience, 95, No. 1, 1–4 (2000).

CAS  Article  Google Scholar 

31.

H. S. Chen and S. A. Lipton, “The chemical biology of clinically tolerated NMDA receptor antagonists,” J. Neurochem., 97, No. 6, 1611–1626 (2006).

CAS  Article  Google Scholar 

32.

E. Scarpini, P. Scheltens, and H. Feldman, “Treatment of Alzheimer’s disease: current status and new perspectives,” Lancet Neurol., 2, No. 9, 539–547 (2003).

CAS  Article  Google Scholar 

33.

R. F. Cowburn, B. Wiehager, and E. Sundström, “Betaamyloid peptides enhance binding of the calcium mobilising second messengers, inositol-(1,4,5) trisphosphate and inositol-(1,3,4,5)tetrakisphosphate to their receptor sites in rat cortical membranes,” Neurosci. Lett., 191, Nos. 1–2, 31–34 (1995).

CAS  Article  Google Scholar 

34.

L. Galla, N. Redolfi, T. Pozzan, et al., “Intracellular calcium dysregulation by the Alzheimer’s disease-linked protein presenilin 2,” Int. J. Mol. Sci., 21, No. 3, 770 (2020).

CAS  Article  Google Scholar 

35.

M. Kawahara and Y. Kuroda, “Molecular mechanism of neurodegeneration induced by Alzheimer’s beta-amyloid protein: channel formation and disruption of calcium homeostasis,” Brain Res. Bull., 53, No. 4, 389–397 (2000).

CAS  Article  Google Scholar 

36.

J. I. Kourie, C. L. Henry, and P. Farrelly, “Diversity of amyloid beta protein fragment [1-40]-formed channels,” Cell. Mol. Neurobiol., 21, No. 3, 255–284 (2001).

CAS  Article  Google Scholar 

37.

T. Iu. Korol’, O. P. Kostiuk, and P. H. Kostiuk, “Effect of beta-amyloid protein on calcium channels in plasma membranes of cultured hippocampal neurons,” Fiziol. Zh., 55, No. 4, 10–16 (2009).

Article  Google Scholar 

38.

I. Žofková, “Hypercalcemia. Pathophysiological aspects,” Physiol. Res., 65, No. 1, 1–10 (2016).

Article  Google Scholar 

39.

P. G. Kostyuk, E. A. Lukyanetz, and A. S. Ter-Markosyan, “Parathyroid hormone enhances calcium current in snail neurones - Simulation of the effect by phorbol esters,” Pflügers Arch., 420, No. 2,146–152 (1992).

CAS  Article  Google Scholar 

40.

J. Zagzag, M. I. Hu, S. B. Fisher, and N. D. Perrier, “Hypercalcemia and cancer: Differential diagnosis and treatment,” CA Cancer J. Clin., 68, No. 5, 377–386 (2018).

Article  Google Scholar 

41.

N. Arispe, E. Rojas, and H. B. Pollard, “Alzheimer disease amyloid beta protein forms calcium channels in bilayer membranes: blockade by tromethamine and aluminum,” Proc. Natl. Acad. Sci. U. S. A., 90, No. 2, 567–571 (1993).

CAS  Article  Google Scholar 

42.

K. N. Green, “Calcium in the initiation, progression and as an effector of Alzheimer’s disease pathology,” J. Cell. Mol. Med., 13, No. 9A, 2787–2799 (2009).

CAS  Article  Google Scholar 

43.

T. Y. Korol, S. V. Korol, E. P. Kostyuk, and P. G. Kostyuk, “β-amyloid-induced changes in calcium homeostasis in cultured hippocampal neurons of the rat,” Neurophysiology, 40, No. 1, 6–9 (2008).

CAS  Article  Google Scholar 

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