Effect of hemic hypoxia on dynamics of GFAP concentrations in the structures of the brain and blood serum of rats
AbstractThis article clarifies the questions on study of hypoxic influence on distribution of filament and soluble forms of GFAP in various structures of the brain (neocortex, cerebellum, hippocampus, striatum, middle brain, pons) and blood of the rats. Quantitative analysis of the contents of GFAP in the brain structures of hypoxic rats has established that hemic hypoxia results in changes in intracellular levels of GFAP forms and also in updating their ratio, which allows one to assume not only a change in astroglial cells, but also testifies to reorganization in the system of intermediate filaments of astrocytes. The level of GFAP substantially changed in all cerebral formations, which was already investigated in the early terms of hypoxic period. Observations showed that hemic hypoxia exerted a varied influence on expression of neurospecific protein in the different structures of cerebrum of rats. Differences in expression of GFAP can be caused by the regional differences in astroglial cellular population, and also their internal features that define the possible answers to hypoxic damage in different functional and morphological structures of the brain. An increase in expression of the investigated form of protein can explain strengthening of astroglial reactivity, a feature of the brain that appears in various types of pathologies of the CNS. Reactive asters in such exhibit hypertrophy and are characterized by an increased level of GFAP, which is an early and reliable indicator of astroglial pathology. An increase in expression of the investigated form of protein may be explained by strengthening of astroglial reactivity, a feature of the brain that appears in various types of pathologies of the CNS. The contents of GFAP in the blood of adult rats, as a result of the hypoxic influence received from it, can indicate a release of GFAP from damaged astrocytes in the blood flow.
Bakhot, C., Armanini, M., Benett, G.L., Wong, W.L., Hansen, S.E., Tavlor, R., 1991. Increase in glia-derived nerve growth following destruction of hippocampal neurons. Вrain Res. 560, 76–83.
Dong, L., Carolyn, L., Frank, C., Ellison, J.A., Lysko, P.G., Li, K., Simpson, A., 1999. Astrocytic demise precedes delayed neuronal death in focal ischemic rat brain. Brain Res. Mol. Brain Res. 68, 29–41.
Duka T.I., Leshchins'ka, I.A., Chornaya, V.I., 2002. The characteristics of glial fibrillary acidic protein – component of astroglial intermediate filaments. Biopolym. Cell 18(3), 179–185.
Duka, T., Duka, V., Joyce, J.N., Sidhu, A., 2009. Аlpha-Synuclein contributes to GSK-3 beta-catalized Tau phosphorylation in Parkinson’s disease models. FASEB J. 23(9), 2820–2830.
Duka, T.I., Leschinskaya, I.A., Chernaya, V.I., 2000. Vliyanie gemichekoy gipoksii sredney tyazhesti na soderzhanie NCAM i GFKB v razvivayuschemsya mozge i mozge vzroslyih zhivotnyih. Reports of the National Academy of Siences Ukraine 4, 164–170 (in Russian).
Erastov, A.A., Vasin, A.L., Ostrovskyi, A.V., Vainer, E.A., Kadomtseva, M.B., Ponomarev, V.N., 1991. Yzmenenye еlektronnykh spektrov porfyrynovykh system pry obluchenyy ympulsnym elektronnym puchkom. Radyobyolohyia 31(6), 900–904 (in Russian).
Gerginova, M., Huckev, D., Ovanesian, M., 1979. Blood gas. Erythropoietic and pathohistological changes in rat chronic methemoglobinemia models. Folia Med. 21(2), 39–43.
Gotham, S.M., Fryer, P.J., Patterson, W.R., 1988. The measurement of insoluble proteins using a modified Bradford assay. Anal. Biochem. 173(2), 353–358.
Hariri, R.J., 1994. Cerebral edema. Neurosurg. Clin. N. Am. 5(4), 687–706.
Houle, J., 1992. The structural integrity of glial scar tissue associated with a chronic spinal cord lesion can be altered by transplanted fetal spinal cord tissue. J. Neurosci. Res. 31(1), 120–130.
Kindy, M.S., Bhat, A.N., Bhat, N.R., 1990. Transient ischemia stimulates glial fibrillary acid protein and vimentin gene expression in the gerbil neocortex, striatum and hippocampus. Brain Res. Mol. Brain Res. 13(3), 199–206.
Lowry, O.H., Rosebrough, H.I., Farr, Z.A., Randall, RJ., 1951. Protein measurement with the folin phenol reagent. J. Biol. Chem. 193(1), 265–275.
Martin, L.J., Brambrink, A.M., Lehmann, C., Portera-Caillau, C., Koehler, R., Rothstein, J., Traystman, P.J., 1997. Hypoxia-ischemia couse abnormalities in glutamate transporters and death of astroglia and neurons in newborn striatum. Ann. Neurol. 42(3), 335–348.
Miller, D.J., Duka, T., Stimpson, C.D., Schapiro, S.J., Baze, W.B., McArthur, M.J., Fobbs, A.J., Sousa, A.M., Sestan, N., Wildman, D.E., Lipovich, L., Kuzawa, C.W., Hof, P.R., Sherwood, C.C., 2012. Prolonged myelination in human neocortical evolution. Proc. Natl. Acad. Sci. USA 109(41), 16480–16485.
Moskalev, J.I., 1991. Otdalennye posledstvija vozdeistvija yoniziruiushcheho izluchenija [Long-term effects of ionizing radiation]. Meditsyna, Moscow (in Russian).
Petito, C.K., Halaby, I.A., 1993. Relationship between ischemia and ischemic neuronal necrosis to astrocytes expression of glial fibrillary acid protein. Int. J. Dev. Neurosci. 11, 237–239.
Schurr, A., Payne, R.S., Miller, J.J., Rigor, B.M., 1997. Brain lactate is an obligatory aerobic energy substrate for functional recovery after hypoxia: Further in vitro validation. J. Neurochem. 69(1), 423–426.
Sharma, H.S., Kretzschmar, R., Cervos-Navarro, J., Ermisch, A., Ruhle-H.J., Dey, P.K., 1992. Age-related pathophysiology of the blood-brain barrier in heat stress. Prog. Brain. Res. 91, 189–196.
Sherwood, C.C., Duka, T., Stimpson, C.D., Schenker, N.M., Garrison, A.R., Schapior, S.J., Baze, W.B., McArthur, M.J., Erwin, J.M., P.R., Hof, P.R., Hopkins, W.D., 2007. Neocortical synaptophysin asymmetry and behavioral lateralization in chimpanzees (Pan troglodytes). Eur. J. Neurosci. 31(8), 1456–1464.
Shimada, M., 1994. Pathogenesis of hypoxic encephalopathy during pre- and perinatal periods. No To Hattatsu 26(2), 111–112.
Sonnewald, U., Westergaard, N., Schousboe, A., 1997. Glutamate transport and metabolism in astrocytes. Glia 21(1), 56–63.
Steward, O., Torre, E.R., Tomasuo, R., Lothman, E., 1991. Neuronal activity upregulates astroglial gene expression. Proc. Natl. Acad. Sci. USA 88(15), 6819–6823.
Yamashita, K., Vogel, P., Fritze, K., Back, T., Hossmann, K.A., Wiessner, C., 1996. Monitoring the temporal and spatial activation pattern of astrocytes in focal cerebral ischemia using in situ hybridization to GFAP mRNA: Comparison with sgp-2 and hsp70 mRNA and the effect of glutamatye receptor antagonists. Brain Res. 735(2), 285–297.