Expression of a Second Ecto-5'-Nucleotidase Variant Besides the Usual Protein in Symptomatic Phase of Experimental Autoimmune Encephalomyelitis
2015
Аутори:
Lavrnja, IrenaLaketa, Danijela
Savić, Danijela
Božić, Iva
Bjelobaba, Ivana
Peković, Sanja
Nedeljkovic, Nadezda
Тип документа:
Чланак у часопису (Објављена верзија)
Метаподаци
Приказ свих података о документуАпстракт:
Ecto-5'-nucleotidase/cluster of differentiation 73 (CD73) (eN) is a
70-kDa glycoprotein expressed in several different mammalian tissues and
cell types. It is the rate-limiting enzyme of the purine catabolic
pathway, which catalyzes the hydrolysis of AMP to produce adenosine with
known anti-inflammatory and immunosuppressive actions. There is strong
evidence for lymphocyte and endothelial cell eN having a role in
experimental autoimmune encephalomyelitis (EAE), but the role of eN in
cell types within the central nervous system is less clear. We have
previously shown that eN activity significantly increased in the lumbar
spinal cord during EAE. The present study is aimed to explore molecular
pattern of the eN upregulation over the course of the disease and cell
type(s) accountable for the induction. EAE was induced in Dark Agouti
(DA) rats by immunization with the spinal cord tissue homogenate and
adjuvant. Animals were sacrificed 8, 15, and 28 days following
immunization (D8, D15, and D28), i.e., at time points which corresponded
to the presymptomatic, symptomatic, and postsymptomatic phases of the
disease, respectively. Significant increase in eN activity and its
upregulation at the gene and the protein levels were demonstrated at D15
and less prominently at D28 in comparison to control. Additionally,
reactive astrocytes abundantly present in the lumbar spinal cord
parenchyma were identified as principal cell type with significantly
elevated eN expression. In all experimental groups, eN was expressed as
a 71-kDa protein band of uniform abundance, whereas the overexpression
of eN at D15 and D28 was associated with the expression of a second
75-kDa eN variant. The possible outcome of eN upregulation during EAE as
a part of protective astrocyte repertoire contributing to the resolution
of the disease is discussed.
Кључне речи:
Ecto-5 `-nucleotidase/CD73; Astrocytes; Neuroinflammation; Adenosine; GlycosylationИзвор:
Journal of Molecular Neuroscience, 2015, 55, 4, 898-911
DOI: 10.1007/s12031-014-0445-x
ISSN: 1559-1166