Expression of Nestin and Glial Fibrillary Acidic Protein in the Marginal Ischemic Zone of the Brain in SHR Rats
- PDF / 3,454,504 Bytes
- 6 Pages / 594 x 792 pts Page_size
- 66 Downloads / 164 Views
576
Cell Technologies in Biology and Medicine, No. 2, August, 2020
Expression of Nestin and Glial Fibrillary Acidic Protein in the Marginal Ischemic Zone of the Brain in SHR Rats D. L. Tsyba1, O. V. Kirik1, M. E. Kolpakova2, A. A. Yakovleva2, and D. E. Korzhevskii1
Translated from Kletochnye Tekhnologii v Biologii i Meditsine, No. 2, pp. 118-124, June, 2020 Original article submitted December 17, 2019 We studied spatial organization and structural characteristics of striatal glial cells in spontaneously hypertensive rats (SHR) in 48 h after 30-min focal ischemia. Immunocytochemical analysis of nestin and glial fibrillar acidic protein (GFAP) revealed 3 types of activated astrocytes: expressing only nestin, only GFAP, or both markers. There were no nestin-immunopositive astrocytes in the striatum of sham-operated rats. In cells expressing nestin and GFAP, localization of these markers did not completely coincide, which can be explained by different functions of these proteins or formation of heterodimers of nestin with other intermediate filament proteins. Key Words: focal cerebral ischemia; nestin; glial fibrillary acidic protein; neural progenitor cells Cerebrovascular diseases are the major cause of global morbidity and mortality after cardiovascular pathology [14]. In Russia, cerebrovascular diseases occupy the second-third place in the general mortality structure. For instance, mortality due to cerebrovascular diseases in 2016 was 190.8 per 100,000 population and 15.95 of all deaths were due to cerebrovascular events [10]. Despite the decrease in mortality from cerebrovascular events to 177,9 per 100,000 population in 2019 (official statistics of the Federal State Statistic Service) [9], this parameter remains high and deserves much attention. In light of this, much efforts should be focused on developing effective measures for the prevention and treatment of acute and chronic disorders of cerebral circulation. Despite impressive progress in experimental modeling of brain ischemia, cellular reactions in the ischemic region remain poorly studied. These reactions determine the degree of nerve Department of General and Local Morphology, Laboratory of Functional Morphology of Central and Peripheral Nervous System, Institute of Experimental Medicine; 2Department if Pathophysiology, I. P. Pavlov First St. Petersburg State Medical University, Ministry of Health of the Russian Federation, St. Petersburg, Russia. Address for correspondence: [email protected]. D. L. Tsyba 1
tissue injury and are thought to be potential targets of neuroprotectors or cell therapy. The possibility of regulating postnatal neurogenesis activated by brain ischemia is of special interest [12]. It was shown that traumatic, inflammatory, ischemic, and other brain injuries activate the pool of neural stem and progenitor cells (NSPC) followed by proliferation and migration of neuroblasts and macroglia to the site of damage [2,6,15,19]. Nestin, intermediate filament protein, is a marker of NSPC. Analysis of its expression together with morph
Data Loading...
