Increased expression of erythropoietin receptor in 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine-induced parkinsonian model

Title:

Increased expression of erythropoietin receptor in 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine-induced parkinsonian model

Creator:

Wu, Y., Sun, X., Feng, X., Liu, R., Huang, L., Shang, Y., Liang, Z., Chen, J., Qiao, X., Liu, C., and Sun, S.

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:00e6a73e-ea8a-4f38-bcd9-93a8080dc661
uuid:00e6a73e-ea8a-4f38-bcd9-93a8080dc661

Subject:

Fyziologie člověka a srovnávací fyziologie, Parkinsonova nemoc, Parkinson's disease, EPOR, MPTP, C57BL/6 mice, ventral mesencephalon, 14, and 612

Type:

article, články, model:article, and TEXT

Format:

print

Description:

Erythropoietin (EPO), known for its role in erythroid differentiation, has been suggested to have a direct protective role against a variety of neurotoxic insults. In the present study, we investigated the expression of EPO receptor (EPOR) and the number of EPORpositive cells in three encephalic regions (ventral mesencephalon, striatum, cortex) following lesion induced by 1-methyl-4-phenyl- 1,2,3,6-tetrahydropyridine (MPTP). C57BL/6 mice underwent intraperitoneal injection of MPTP at 24 h intervals for 5 days, and their brains were examined 1, 2, 4, 7, 14 or 21 days after the last injection. Western blot and immunohistochemistry analysis revealed that EPOR was dramatically up-regulated in the ventral mesencephalon, 4 days after MPTP insult until the day 21. In contrast, there was a baseline level of EPOR in the striatum and cortex. At subsequent time points after MPTP injury, the levels of EPOR in the two regions were not statistically different compared with those in normal animals. These results suggest that the regional specific up-regulation of EPOR at an early stage after MPTP stimulus may represent a pro-survival mechanism against neurotoxin injury in Parkinsonian model., Y. Wu ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy

Language:

English

Rights:

http://creativecommons.org/licenses/by-nc-sa/4.0/
policy:public

Source:

Physiological research | 2010 Volume:59 | Number:2

Harvested from:

CDK

Metadata only:

false